Swelling Of Foot After Pedicure

genetic diseases caused by mutation in the genes are presented with a very low frequency (4), but they are responsible for inherited conditions that usually affect significantly the quality of life of patients. They also have a considerable impact at the household, not only by the level disabling, but the anxiety that leads transmit to future generations.

The Korea or Huntington disease (HD), also known as Mal de San Vito, is an example of these hereditary diseases. Was recognized in 1872 by the American physician George Huntington Summer (4,5,8), based on a study of a mother and daughter who had choreic movements, progressive mental deterioration and suicidal tendencies (4). Huntington's Disease is not the only existing hereditary chorea (8), so the only way to make a definitive diagnosis is by a karyotype.

patient with Huntington's Disease Taken from youtube.com

http://www.youtube.com/watch?v=OveGZdZ_sVs

The prevalence is estimated between 5 and 10 people affected per 100,000 inhabitants, among populations EuropaOccidental and descendants (10). Not enough data to estimate the incidence in Costa Rica (10), however, they have been conducted that have confirmed certain hereditary characteristics of the disease (10). For 2007, it had conducted tests of 38 Costa Rican belonging to 4 different families. Of these individuals, 7 had a clinical diagnosis of HD and 18 had the characteristic mutation Huntingtons (10).



Etiology Genetic diseases are caused by mutations that can occur at the level of the genome, chromosome or genes (4). They are the result of imperfections that occur by chance in the DNA replication process or because of the physical or chemical agents (6). The level of gene mutation occurs with a very low frequency (4), however, there are cases where the injury is not resolved genes and thus is transmitted to the next generation.

The mutational mechanism responsible for Huntington's disease is known as trinucleotide repeat expansion (4). There is evidence that originates along the mitotic divisions of germ cells (4) (gametes). The mutation is unstable (4.6), which means that the size of the repeated sequence varies when cells divide (10).

In the case of Huntington, the trinucleotide CAG (cytosine-adenine-guanine) (4.10) is repeated over 36 times in a gene called HD10 or IT15. This gene is located on the short arm of chromosome 4 (4p16.3) and is responsible for producing a protein called huntingtin (htt) (4.10). The function is still unknown (4), but is highly expressed in the brain, mainly in the cytoplasm (4,10). The mechanism causing expansion and the way that leads to neurodegeneration is one of the many aspects of the htt protein has not been explained so far (4,10).

Figure # 1
Scheme with the location of the HD gene
Taken from Genetics Home Reference
http://ghr.nlm.nih.gov/gene=htt

mutant htt protein is completely dominant (4) and given that the affected chromosome belongs to the autosomes (sex chromosomes), it is said that this disease has an autosomal dominant inheritance pattern (4,6,10).

All individuals inherit the mutated allele will eventually develop the disease unless they die of other causes before the onset of symptoms (10).

The number of repeats influences the degree of neuronal degeneration and the age at which symptoms begin to manifest. A normal person is between 6 and 36 repeats (4.10). The greater the number of repetitions, the greater the degree of injury observed in the striatum (4).

The age of onset is inversely proportional to the number of CAG repeats (4,10). The more repetitions of the trinucleotide chain are present, the age of onset is lower. This pattern was confirmed in study in Costa Rica (10).

expansions between 40 and 50 CAG repeats are often seen in people with symptoms between 30 and 50. Juvenile HD is associated with cases that exceed the 70 repetitions (10). Unfortunately, current knowledge of Huntington's disease can not yet accurately predict when the symptoms will appear (10).

Another pattern that is currently studying the relationship between the parent inheriting the mutated gene and the number of CAG trinucleotide repeats. When the transmission is matrilineal, the allele is of equal or smaller size (fewer repetitions). When paternal transmission is the mutation in the child tends to be larger (more repeats) (4:10).

Detection of carriers of the disease in presymptomatic phases is now possible by molecular biology techniques (4). Although there are certain legal and ethical use of genetic counseling in these cases, it should be noted that enables parents to calculate the probability of having a son or daughter who will develop HD. Pathology



Although the mutant protein found in many places along the Centra Nervous System (l, 4), neurodegeneration appears specifically in the striatum (1,4,5,8,10 ) and cerebral cortex (l, 4,10,11). The reason why the injuries were concentrated in these areas is unknown (4).

The Corpus striatum is part of the basal ganglia, which are a group of interconnected gray mass nuclei involved in motor functions and non-motor (1). Found in the deep white matter of each cerebral hemisphere. Some texts refer to as the basal ganglia, however that term is not used by most neuroscientists (9).

The basal ganglia are mainly associated with the beginning and end of voluntary and involuntary movements (9), and the control of the adjustments required by them (11).
no motor function of the basal ganglia is related to cognitive processes and emotion (1). The lesions in these nuclei produce movement disorders such as chorea, athetosis, ballism, dystonia and tics. Note the difference with lesions in the cerebral cortex that usually cause total loss of movement (1).

The Corpus striatum consists of three cores called: caudate, putamen and globus pallidus (1.9).

Figure # 2
Scheme with the location of the basal ganglia
IMBIOMED Taken
http://www.imbiomed.com.mx

the caudate nucleus is a C-shaped structure that is higher than the thalamus. Has three parts: head, body and tail (1). The head of the caudate nucleus is in contact with one wall of the lateral ventricle.

is associated with the limbic system (9), especially anteriorly. For this reason it is said that is related to emotions such as anger, pleasure, docility and affection (9). Some studies indicate that the activity of neurons in this nucleus can be seen by eye movements (9) and is also associated with cognitive processes processes (11).

the putamen and globus pallidus are lateral thalamus and separated from it by the internal capsule. The putamen is closer to the cortex while the globus pallidus is deeper. The activity of neurons in the putamen preceding body movements (9), especially arms, legs and face. The globus pallidus is involved in the regulation of muscle tone in certain movements. These two nodes form a structure known as lenticular nucleus.

In advanced stages of Huntington's disease shows dilatation of the frontal horns of the lateral ventricles and the ventricles characteristic Wagon (4) (atrophy of the caudate head). Also observed retraction of dendrites, predominantly in the cerebral cortex (l, 4). While in the basal ganglia atrophy explains the movement disorders, the lesion in the cerebral cortex to an explanation of psychiatric problems, including dementia. Associated progressive personality changes (5).

Figure # 3

HD Impact (above) in the basal ganglia vrs normal brain (bottom)
Taken from Folding @ home
http://folding.stanford. edu / Inglés / FAQ-Diseases

The rest of the basal ganglia (Claustrum (2), amygdaloid nuclei, Subthalamic nucleus, substantia nigra and red) do not seem to be affected by Huntington's Disease, however it is related to other diseases where there are movement disorders such as Parkinson's (1). Pathophysiology



As mentioned above, the CAG trinucleotide expansion leads to the emergence of mutant htt protein with an abnormal aggregation capacity is directly proportional to the number of repetitions (4). The presence of this mutated protein and subsequently alter the dendrite neuronal death occurs by apoptosis (4). There is evidence of neuronal dysfunction in the body initially Striatum. In advanced stages of the disease is found atrophy, especially in the putamen (4).

Figure # 4
gliosis in the striatum, patients with HD (left) vrs. normal (right) Taken
Neuropathology
http://neuropathology.neoucom.edu/chapter9/chapter9eHD.html

pathological lesions are also characterized by proliferation of astrocytes in the central nervous system (gliosis .) Some authors specifically mention the process of reactive astrocytosis (4). Astrocytes are the largest cells of the neuroglia (1) (CNS supporting cells). It is thought that these cells are related to the healing of damaged tissue (1).

Physical and Psychological Symptoms

Huntington's disease, cognitive and psychiatric disorders tend to occur months or years before the other (4.5). Studies have explored the possibility of detecting neuropiscológico deficit when the patient is still pre-symptomatic (5), however it is difficult to make a proper diagnosis only with psychological tests.

The framework of cognitive and psychiatric disorders is variable (4.5), and ranges from subtle changes in personality to psychotic disorders (4). The literature review cites the following signs:

- Depression (4.8)
- Irritability (4.8)
- Reduced memory (4,5,10)
- Loss of self-criticism (4)
- Distractibility (3 , 4)
- mood changes (4.5)
- Anxiety (4)
- Apathy (4)
- Aggression (4)
- Insomnia (3.4)
- Hallucinations (4)
- suicidality ( 4)

Dementia is progressive (4,5,8,11) and ends up being global in advanced stages (4.5) and is established which is of subcortical type (3,4,5). This type is characterized by disturbances in the ascending reticular activating system (3), which is responsible for controlling the states of arousal, alertness and attention (1) and has a central role in the selective recognition (1). These features explain the distractibility, insomnia, and to some extent cognitive problems (1.3).

studies in this type of dementia indicate that the patient has difficulty initiating the process of attention and easily distracted (3). The answers may be successful but require a lot of time to produce (3).

physical manifestations are characterized by choreic hyperkinesias (1,4,8,10). Chorea is a movement disorder where there are sudden jerky, fast, frequent and involuntary (1,4,5,10), in the case of HD, the movements are messy, arrhythmic, and messy (4) in the extremities and trunk. The literature review cites the following signs:

- choreic movements of the limbs (1,4,8,10)
- Head Spins (1.4)
- protrusion of the tongue (4)
- Gesturing face (grimacing) (1,4,10)
- Lift Shoulders (4)

minor motor abnormalities include:

- Restless (4)
- eye movements (4)
- Nystagmus (4)
- hyperreflexia (4)
- Dysarthria (4.5)
- Dysphagia (4)
- Athetosis (4.11)
- rapid and excessive movements of the fingers (4) Diagnosis and

prodnóstico

Clinical diagnosis is based on the presence of a positive family history and testing of transmission of the disease in heritable (4). The installation of a progressive motor disability, mental disorders and neuroimaging (4).

Figure # 5

HD patient with magnetic resonance (top) vrs. normal subject (bottom)
scielo.br Taken
http://www.scielo.br/img/revistas/bjmbr/v39n8/html/6233i01.htm

In some cases it is possible to detect subtle alterations in cognitive and motor (4), however, definitive diagnosis can only be done by genetic testing (4).

When genealogical research is positive, the differential diagnosis must be made to:

Sydenham's chorea: a benign (1.4), there is atrophy of the caudate nucleus (4) and is caused by rheumatic fever (1). Is rapidly evolving. Vascular

Korea: filed at a later age and there is no hereditary factor (4). No psychiatric accented (4). Tendency to spontaneous improvement (4).

Infectious Koreas, caused by measles, smallpox, typhoid fever. Have an abrupt onset and gradual evolution is often localized and the absence of mental disorders (4). Koreas

Tumor: No heredity and mental disorders in the early stages (4). Their evolution is rapid and localized (4).

Wilson's disease: is presented at an earlier age, no dementia, presence of liver disease (4).

choreic syndrome secondary to injury: Outcome of trauma or drug ingestion, hyperthyroidism, stroke or encephalitis (4)

In advanced stages, patients lose their physical capacity mental and personal care. The march is difficult and swallowing problems (4). Death occurs pro complications from general weakness (4), usually between 10 and 25 years have shown the first symptoms (4). Patients do not die of Huntington's disease, died with the disease.

Treatment and Genetic Counseling

The current treatment of this disease is limited to alleviating some of the expressions (4). It is not possible to delay the onset or progression of symptoms (4). Usually provides support to paciete and their families (4). It seeks the participation of doctors, psychologists and therapists, especially to help the understanding of neuropsychiatric symptoms and offer a better quality of life for the patient (4).

Certain drugs used to treat dementia may be useful (4,7), yet none of them are considered truly effective for efficient treatment or other mental disorders.

From the point of view of genetic counseling, it is now possible to detect carriers of the disease (4). Even in Costa Rica is possible to perform these tests (10). Although the application of these techniques still has certain legal and ethical (4), have the advantage that help ease the anticipation and uncertainty, especially for people who want to know if the children are at risk of developing the disease (4).

Prenatal diagnosis is very controversial especially in countries where sex-selective abortion (4). Some scientists have found cases where some family members prefer not to know their carrier status (4).

In the study conducted in Costa Rica (10), participants were given continuous support during the process of deciding whether or not undergoing genetic testing, whether or not to know the outcome. Some of the positive cases are being followed by neurologists and psychologists. Original Paper



This research was part of Neuroanatomy course at American University. made by Katherine Chacón, Montserrat Alvarado, Karla Camacho, Angelica Garita and Leo Melendez.

Disposible online:
http://www.bluejaygallery.com/download/EnfermedadHuntington.pdf



References (1) Afifi, Adel. Ronald Bergman. 2006. Functional Neuroanatomy. 2nd. Edition. Editorial McGrawHill. Mexico. Cap 13.

(2) Crick, Francis. Kosh, Christof. 2005. What is the function of the claustrum?. Philosofical Transactions. (2005) 360, 1271-1279.

(3) Coello, Ramiro. Garcia, Angel. Nunez, Maria Isabel. 1980. A Case of Functional subcortical dementia. Honduran Medical Journal. Vol 48.

(4) Encinosa, Guianeya. 2001. Huntington's chorea. Journal of Human Genetics. Volume 3, Number 1. `

(5) Gadea, Marlen. Espert, R. Chirivella, Javier. 1996. Presymptomatic detection of neuropsychological deficits in Huntington disease: controversies. Behavioral Psychology. Volume 4, Issue 3. 363-375.

(6) Jaramillo, Juan. 2003. What the doctor should know about genes. Acta Médica Costarricense. College of Physicians and Surgeons. Volume 45, Number I.

(7) Jimenez, F. Toledo, M. Puertas, I. Lefty B. Barcenilla, B. 2002. Olanzapine improves chorea in Huntington disease patients. Journal of Neurology. 35 (6). 524-525.

(8) Royuela, A. Gil, A. Macías, 2003. J. A case of obsessive Symptoms in Huntington's disease. Actas Esp Psiquiatr. 2003, 31 (6). 367-370.

(9) Tortora, Gerald. Derrickson, Bryan. 2006. Principles of Anatomy and Physiology. 11 th. Edition. Editorial Médica Panamericana. Mexico DF. Mexico. Cap 14.

(10) Vasquez, Melissa. Morales, Fernando. Fernandez, Hubert. Del Valle, Gerardo. Fornaguera, Jaime. Cuenca, Patricia. 2007. Molecular diagnosis of Huntington's disease in Costa Rica. Acta Médica Costarricense. College of Physicians and Surgeons. Volume 50, Number I.

(11) Young, Paul. 2001. Clinical Functional Neuroanatomy. First Edition. Editorial Masson. Spain. Chapter 8.

Women In Girdles, Stockings & High Heels

Huntington's chorea CSF

The cerebrospinal fluid (CSF), also known as cerebrospinal fluid (1) is a clear, colorless substance that protects the brain and spinal cord of physical and chemical damage. It also carries oxygen and glucose from the blood to neurons and glia (2). CSF continuously circulates through the cavities of the brain and spinal cord in an area called "subarachnoid. Both cerebral and spinal level, this space is between the arachnoid and pia mater meninges.

Figure # 1: Diagram with the meninges at the level of spinal cord
wikispaces.com Taken
http://lamedulaespinal.wikispaces.com/2.+CONFIGURACI% C3% 93N + DE + LA + M. + E.

fluid consists of water (main constituent), protein, glucose, cells, electrolytes and peptides (1)

CSF examination is of great value in neurologic diagnosis. Lumbar puncture, performed at the L3-L4 vertebrae can extract liquid for purposes of analysis, measuring the pressure or introduce therapeutic agents, anesthetics or contrast material (3).

This liquid is known for a long time. The Egyptians documented the presence of intracranial fluid in Ebers Papyrus (1500 BC). Hippocrates (450 BC), also described some conditions associated with excess water inside the skull (4). Features



CSF helps to maintain an internal condition of balance (homeostasis) in the Central Nervous System (2). Has three main functions

1. Mechanical protection: Represents a medium that absorbs shocks received by the skull and vertebrae. This means that helps protect the nerve tissue of the spinal cord and brain. The latter essentially "floats" in the cranial cavity (2).

2. Chemical Protection: Provides an optimal chemical environment for the transmission of impulses at neuronal (2). Its composition is relatively stable, even when there are noticeable changes in the chemical structure of plasma. (1)

3. Circulation: The CSF allows the exchange of nutrients and waste products between blood and nervous tissue (2).

Figure # 2: Diagram with the ventricles in the brain
lookfordiagnosis.com Taken
http://www.lookfordiagnosis.com/mesh_info.php?term=ventr% C3% ADculo + side & lang = 2

Training Most of the LCR (60%) is produced by the choroid plexus (1), especially those found on the roof of the third ventricle. These plexuses are a network of capillaries (blood vessels) on the walls of the ventricles. The capillaries are covered in turn by ependymal cells are ultimately those that generate CSF from blood plasma (2). Ependymal cells have very close bonds, therefore, the substances that pass from plasma to CSF \u200b\u200bshould be through them. The barrier formed by the ependymal cells prevents the ingress of undesirable elements and the LCR called Hematocefalorraquídea Barrera (2).

Some authors explain the formation of CSF as an "ultrafiltration" of plasma, however recent evidence attributed their formation to the processes of diffusion and active transport (1). In that there is consensus is that it occurs at a rate of 0.35ml per minute (20ml/hr). If the normal volume in adults is 100 to 150ml, then estimated that the CSF is replaced every 5 - 7 hours (1) (2) (4).

Other CSF production sites, such as the pial brain surface, brain intracellular space and perineural space (1). Resorption



CSF is gradually reabsorbed into the blood by the arachnoid villi. These in turn are projected onto the dural venous sinuses, especially in the superior sagittal sinus. In this cluster is called arachnoid granulation or Pacchioni (2).

alternative sites have been reported resorption (1) such as the arachnoid membrane, sleeves roots cranial and spinal nerves (1) (5), the capillary endothelium and choroid plexus even themselves.

Normally, the fluid is reabsorbed as fast as it is formed in the choroid plexus (20 ml / hr), which makes the pressure remains constant.

Animation CSF Circulation Taken from youtube.com

http://www.youtube.com/watch?v=JCf273U0ktc

Circulation

The mechanism that moves the CSF through its route is not fully understood (5), however there is consensus that most of the liquid flowing the following structures (1) (2):

a. Lateral ventricles
b. C.
foramen of Monro D. Third Ventricle
Cerebral aqueduct of Sylvius or foramen
e. Fourth ventricle
f. Magendic hole (central) and holes
Lushka g. Subarachnoid Space of the Brain and Spinal Cord

There are several factors that contribute to their movement are the following (1):

1. Momentum: The movement of CSF from the areas where it occurs to areas where it is absorbed. This process is called diffusion of CSF positive balance areas to areas of negative balance (1). Some authors indicate that the fluid is mobilized to the nearest point of resorption, implying that there is no flow in the conventional sense (4).

2. Swing: The CSF is in continuous state of oscillation, with swinging movements whose amplitude increases as the liquid approaches the fourth ventricle (1).

3. Pulsatile Movement: Usually described rhythmic movements synchronized with the arterial pulse. It is thought that these oscillations are caused by the expansion of the brain and arteries during systole rather than by pulsations of the choroid plexus as previously believed (1). In fact, these palpitations occur almost simultaneously with the intracranial pulse (150 msec in the cardiac cycle). In the atlas of anatomy can be seen that there are irrigation and drainage at that level, for example, the anterior spinal vein, located in the anterior median fissure (6). There

an additional factor, although it has not been scientifically proven, may be related to CSF \u200b\u200bcirculation. We refer to the difference in the density of the liquid at the ventricular and lumbar level. The protein quantitative analysis shows that the concentration of albumin increased 2.2 times from the ventricular to lumbar CSF LCR (4). This means that the liquid along with proteins tends to decrease, which in turn cause an upward momentum part of it.

To read more

(1) Afifi, Adel. Ronald Bergman. 2006. Functional Neuroanatomy. 2nd. Edition. Editorial McGrawHill. Mexico. Cap 29.

(2) Tortora, Gerald. Derrickson, Bryan. 2006. Principles of Anatomy and Physiology. 11 th. Edition. Editorial Médica Panamericana. Mexico DF. Mexico. Cap 14.

(3) Young, Paul. 2001. Clinical Functional Neuroanatomy. First Edition. Editorial Masson. Spain. Cap 2.

(4) Wilson, E. Oehninger, C. 2007. Evolution of Knowledge from Antiquity CSF to the Present Day. Archives of the Institute of Neurology. Volume 10, Number 1-2. Online. Date of Consultation: 19/Nov/2009.
Available at:
http://archivos.institutodeneurologia.edu.uy/2007/contenido.php

(5) Killer, H. Jaggi, G. Flammer, J. Miller, N. Huber, A. Mironov, A. 2006. Between Cerebrospinal fluid dynamics and the intracranial subarachnoid space of the optic nerve. Brain (2006). Online. Date of Consultation: 19/Nov/2009.
Available at:
http://brain.oxfordjournals.org/cgi/reprint/130/2/514.pdf

(6) Netter, Frank. 2007. Atlas of Human Anatomy. 4 ª. Edition. Editorial Masson. Barcelona, \u200b\u200bSpain. Lam 173.

Scar Tissue Removal Knee Surgery

The basal ganglia are a group of interconnected gray mass nuclei involved in motor and non motor functions ( 1). Found in the deep white matter of each cerebral hemisphere. Although it is understood as the joint ganglion cell bodies outside the central nervous system, basal ganglia are an exception to that rule. Some texts still refer to as the basal ganglia, however that term is not used by most neuroscientists (2).

Figure # 1: Diagram of Front Court, Right Hemisphere

The basal ganglia are mainly associated with the start / end of voluntary movements (2) and control settings associated the same (3). Lesions in these areas cause movement disorders such as chorea, athetosis, ballism, dystonia and tics; Note the difference with lesions in the cerebral cortex that usually cause total loss of movement (1). No motor function of the basal ganglia is related to processes cognition and emotion (1).

Figure # 2a: Front Court
Brain Taken http://www.anatomiahumana.ucv.cl/efi/modulo21.html

Figure # 2b: Cross section of brain

http://www.anatomiahumana.ucv.cl/efi/modulo21.html Taken

Figure # 2a and # 2b will be used later to locate the different cores. Both the front and cut in cross section can be seen as a reference the following important structures: Corpus Callosum (point 9), thalamus (item 11), the lateral ventricle (point 12), internal capsule (point 1), the external capsule (point 2) and third ventricle (7). Caudate Nucleus



the caudate nucleus is a C-shaped structure and is higher than the thalamus (Figure # 1). Has three parts: head, body and tail (1). The head of the caudate nucleus is in contact with one wall of the lateral ventricle (Figure # 2, point 4).

is associated with the limbic system (2), especially the anterior (Head). For this reason it is said that is related to emotions such as anger, pleasure, docility and affection (2).

Some studies indicate that the activity of neurons in this nucleus can be seen by eye movements (2) and could be also associated with cognitive processes (3). Lenticular Nucleus



the lenticular nucleus comprises the putamen and globus pallidus (Figure # 1). The putamen is closer to the cerebral cortex (Figure # 2, Item 5) while the globus pallidus is more close to the thalamus (Figure # 2, point 6).

The activity of neurons in the putamen precedes body movements (2), especially arms, legs and face (1). The globus pallidus is involved in the regulation of muscle tone in certain movements.

the lenticular nucleus, together with the caudate nucleus form the corpus striatum.

Figure # 3: Cross Section of the brain
From Wikipedia
http://en.wikipedia.org/wiki/Claustrum

Claustrum
The Claustrum is
a thin core is located between the putamen and cerebral cortex. Little is known about its function (4). It is believed to be associated with the state of awareness and coordination of cortical regions, but none of this has been demonstrated (4).


amygdaloid nuclei amygdaloid
The core is located in the temporal lobe, near the uncus is considered part of the limbic system, through their connections can influence the body's response to environmental changes. For example, feelings of fear, you can change the heart rate, blood pressure, respiratory rate, skin color. Also associated with the autonomic nervous system and is related to visceral functions, such as the production of HCL. Subthalamic nucleus



The subthalamic nucleus is the mass of the larger nuclear subthalamus (3). It is located anterior to the lateral thalamus and the hypothalamus, including the substantia nigra and red nucleus (Figure # 1).
This core is associated with control of involuntary movement. Injuries to this area produce tics and hemiballism contralateral (3).

Some authors do not consider the subthalamic nucleus as a basal ganglion, however, from the functional point of view should include (1).

substantia nigra and Red

The substantia nigra is the largest nuclear mass in the midbrain (3). Is lower than Subthalamic nucleus (Figure # 1). The black color of the substance is due to neurons that are loaded with melanin.

is associated with movement control and an injury is usually manifested by stiffness (resistance to passive movement) and tremors. Parkinson's disease, characterized by a fine, rhythmic movement, is caused by a decrease in deposits of dopamine, especially in the substantia nigra (1).

Some authors do not consider the substantia nigra and basal ganglia as a Red. Like the subthalamic nucleus, should be included from the functional point of view (1).

To read more:

(1) Afifi, Adel. Ronald Bergman. 2006. Functional Neuroanatomy. 2nd. Edition. Editorial McGrawHill. Mexico. Cap 13.

(2) Tortora, Gerald. Derrickson, Bryan. 2006. Principles of Anatomy and Physiology. 11 th. Edition. Editorial Médica Panamericana. Mexico DF. Mexico. Cap 14.

(3) Young, Paul. 2001. Clinical Functional Neuroanatomy. First Edition. Editorial Masson. Spain. Chapter 8.

(4) Crick, Francis. Kosh, Christof. 2005. What is the function of the claustrum?. Philosofical Transactions. (2005) 360, 1271-1279. Online. Accessed: 18/Nov/2009.
Available at: http://www.klab.caltech.edu/news/crick-koch-05.pdf