Attention Deficit Hyperactivity Disorder (ADHD) is a disorder characterized by hyperactivity, short attention span and impulsiveness (insufficient impulse control). ADHD is one of the most common reasons for referrals to child and adolescent mental health and diseases departments. It is a chronic disorder that starts in pre-school childhood and can progress with different findings in adult life. If left untreated, its symptoms negatively affect almost every aspect of the child’s education and life, leading to intense mental, social and school problems.
ADHD was not well defined until the last 30 years, and there has been an intense increase in scientific reports on this subject in the last three decades. After the outbreak of encephalitis laterjika in World War I, a postencephalitic behavioral syndrome characterized by hyperactivity, coordination disorder, learning difficulties, impulse control problems and aggression has been described in some children and adolescents. In 1947, Strauss et al. reported that children with hyperactivity, confusion, impulsivity, perseveration and cognitive impairment had brain damage that could not be shown later, and they named this condition as “Minimal Brain Injury Syndrome”. In the 1960s, the definition of “minimal brain dysfunction” was used for this group of children who did not have a defined neurological disorder.
For the first time, the diagnosis of “hyperkinetic reaction” was included in the DSM-II (Diagnostic and Statistical Manual of Mental Disorders), the American system for the Diagnosis and Classification of Psychiatric Disorders, in 1970. In 1980, the term “attention deficit disorder” was used in the DSM-III and it was divided into two groups as hyperactivity and non-hyperactivity. In 1987, the term “attention deficit hyperactivity disorder” was introduced in the DSM-III-R. In 1994, ADHD is given under the general title of “Attention Deficit and Disruptive Behavior Disorders” in DSM-IV. This group includes Attention Deficit Hyperactivity Disorder, Conduct Disorder, Oppositional-Defiant Disorder, and Disruptive Behavior Disorder Not Otherwise Specified. These three basic disorders can also be defined as expression disorders. According to DSM-IV, there are three types of ADHD: 1. Attention deficit type, 2. Hyperactivity and impulsivity type, 3. Combined type.
Epidemiology
ADHD is observed in approximately 3-5% of school age children. It is stated that there is limited information about the frequency in adolescents and adults. Its incidence is higher in boys than in girls, and the male/female ratio is reported to be between 3-5/1. It is thought that ADHD is overlooked or ignored because girls are more likely to have inattention and cognitive difficulties, and have less aggressivity and aggressive behavior problems. Because men show aggression, aggression and behavior disorders more frequently, they are more frequent and earlier to be brought to outpatient clinics.
Onset is usually around the age of 3, but the primary school years are the most suitable time, when the attention span and concentration required for education and training are expected to make a diagnosis.
Etiology
ADHD is a heterogeneous disorder of unknown cause. Conditions such as fragile-X, fetal alcohol syndrome, very low birth weight, and, less frequently, thyroid disorders of genetic origin, present with ADHD symptoms. However, such cases constitute a very small proportion of all children with ADHD. Some possible reasons are suggested in the studies on the subject:
a. Genetic causes
b. Brain injury
c. Neurotransmitters
d. Food-additives and toxic substances
e. Psychosocial factors
a. Genetic Reasons:
Genetic relationship and data were obtained for the first time from studies conducted with relatives of these children. This disorder is 4-5 times more common in first-degree relatives of children with ADHD. Family studies, especially with first and second degree relatives, reveal that antisocial personality disorder, hysteria, alcoholism and substance use are more common in families of hyperactive children.
Most significant data on the relationship of ADHD to the genetic aspect have been obtained from twin studies. It has been suggested as genetic evidence that monozygotic twins have more concordance than dizygotic twins or that siblings of hyperactive children have twice the risk compared to the general population. It is known that genetic transmission is 51% in monozygotic twins and 33% in dizygotic twins. Adoption studies also support familial transition.
No specific gene has been found at this point, but research is ongoing. The mode of genetic transmission is thought to be unigenetic rather than polygenic as previously suggested. Many studies have suggested that mutations in several genes that affect the prefrontal cortex and basal ganglia cause ADHD. Some studies point to genes encoding dopamine receptors and transporters. These genes are very active in the prefrontal region and basal ganglia. Mutations in dopamine receptor genes make dopamine receptors less sensitive to dopamine. Conversely, as a result of mutation of dopamine transporter genes; Few carriers are secreted. Children with ADHD are likely to have a particular variation in the dopamine transporter gene DAT1 more often than those without. Similarly, a variant in the dopamine receptor gene D4 has been found to be more common in children with ADHD.
In a study conducted with children with ADHD and Tourette’s disorder and their families, it was suggested that genetic transmission may occur as semi-recessive and semi-dominant with the gene related to serotonin metabolism.
b. Brain Damage:
Since the disease was defined, it has been stated that these children have minimal, occult or overt central system damage in the perinatal period. There may be toxic, metabolic, mechanical and circulatory causes causing this damage, as well as infections affecting the CNS in early infancy. It has been reported that the rate of premature birth is also common and physical damage to the developing nervous system is present in the prenatal period. The presence of faint neurological symptoms and some learning disorders together, the possibility of developing non-specific EEG disorders and epilepsy more than normal are evidence of brain damage.
Neurophysiology and Brain Imaging Studies:
A significant proportion of children do not have any signs of structural damage in the CNS. In the last 10 years, imaging studies have yielded findings indicating that individuals with ADHD may have functional disorders in their brain regions. In these studies, it is suggested that at least two of the basal ganglia formed by the prefrontal cortex, cerebellum and nerve cell clusters deep in the brain are involved. In studies, the right prefrontal cortex and two basal ganglia (nucleus caudatus and globus pallidum) were found to be significantly smaller than normal in children with ADHD. In another study, the vermis region of the cerebellum was found to be smaller in children with ADHD.
These findings support the theory that there may be a defect in frontal lobe development and function in ADHD. It has been reported that the main deficiency in ADHD is the difficulty in inhibiting responses, and this may be related to the outside of the dorsoleteral part of the prefrontal cortex. In SPECT (Single Photon Emission Tomography) studies, a decrease in regional blood flow in citratum and an increase in sensory and motor regions were observed. In PET (Positron Emission Tomography) studies, it has been observed that there is a decrease in cerebral blood flow and metabolic rate in the frontal lobes of children with ADHD. Regarding the neurophysiological causes of the disorder, it is emphasized that there may be delays or disruptions in the development of the CNS. In addition, it is mentioned that the suppressive effect of the frontal lobe on the lower centers is impaired or not, and the effect of the reticular activating system (RAS) on the attention center is reduced.
The striking point in these imaging results; Most of the regions specified as small in size in children with ADHD are areas that regulate attention. The right prefrontal cortex plays a role in preparing a behavior, filtering irrelevant stimuli, and developing self-awareness of time and self. The caudate nucleus and globus pallidus prevent automatic responses to more careful designs created in the cortex and coordinate neurological inputs between various regions of the cortex. The role of the vermis region is not entirely clear. However, early studies suggest that it may have a role in regulating motivation.
Executive Functions:
As a result, behavioral inhibition and self-control are impaired as a result of central deficiencies in ADHD. Self-control is the capacity to inhibit (suppress) or delay initial motor (perhaps emotional) responses to an event. Self-control is fundamental to success in any task. Many children gain mental activities called executive functions as they get older. These functions prevent drifting away from the purpose, remind the goals and enable to pass the necessary stages to reach the goal. To achieve purpose in a business or game, one must have the ability to set the goal. Foresight, controlling emotions, and motivation are essential to achieve the goal. A person cannot successfully perform any of these functions unless they are able to control their thoughts and impulses. Executive functions are acquired externally at an early age. The child can talk aloud to himself while remembering a task or solving a problem. However, as they get older, it becomes internalized, individualized and difficult for others to understand. The regulations necessary for the fulfillment of these executive functions in children with ADHD are lacking.
Executive functions are grouped into 4 mental activities: one of them is working or working memory. This is keeping information in mind during any task or study. Such recollection is crucial to timely and purposeful behavior. The result is inference, foresight, preparation, and imitation from complex and novel behaviors. All these are impaired in children with ADHD.
Internalization of self-directed speech is another executive function. Before the age of six, most children speak aloud when performing a task or solving a problem to remind themselves how to do it. For example, “Where did I put my book?” Like “Oh, I put it under the bench”. In early primary school this particular speech is inaudible murmuring and usually disappears by the age of 10. Internalized, self-directed speech provides self-reflection; In order to follow rules and guidelines, conclusions are drawn by understanding previous rules and using self-inquiry as a form of problem solving. In a study, it was reported that the internalization of self-directed speech was delayed in children with ADHD.
Third executive mental function; control of emotions, motivation and alertness. The final executive function is reconstitution. It is breaking down the observed behavior into parts and putting these parts together in new activities. Restructuring gives people fluency, flexibility and creativity. Thus, the person reaches the goal by passing all the necessary steps. Studies indicate that children with ADHD have less restructuring ability than other children.
In studies determining the level of arousal, it has been determined that these children tend to respond to stimuli below the arousal threshold, for example with galvanic skin stimuli or evoked potential.
c. Neurotransmitters:
Neurotransmitters are also examined based on the effects of drugs used in treatment. Since amphetamines, the most commonly used drugs, affect both dopamine and norepinephrine, it has been suggested that there may be dysfunction in both systems. Many studies indicate low levels of CSF circulation and receptor sensitivity of dopamine and possibly norepinephrine in ADHD.
Dopamine is released from specific regions of the brain. In particular, it inhibits (suppresses) or regulates the activities of other neurons related to emotion and behavior. Dopamine receptors are located on the surface of certain neurons. Dopamine transmits the message by binding to the receptor of the other neuron.
There are also reports about low serotonin levels recently.
d. Food and Additives:
Although it is suggested that food additives such as dyes and preservatives, sugars or lead may cause this disorder, there is no scientific evidence about them.
e. Psychosocial factors:
Preparatory and accelerating effects can be mentioned rather than a basic effect in the development of the disorder. It has been reported that children with ADHD often come from broken families, the rate of being the only child or the first child is higher than the controls due to the constant incompatibility of the parents and psychiatric disorders in the parents. It has been observed that children in orphanages have short attention spans and are hyperactive. These symptoms are due to long-term emotional deprivation and disappear with the improvement of the situation, such as the adoption of the child.
It is generally thought that biological and psychosocial factors play a role in ADHD.
Risk Factors for ADHD
• The mother’s before or during pregnancy:
• medical condition
• emotional problems
• smoking
• drinking alcohol
• birth complications
• Child’s history:
• moderate head injury (significant association)
• less breastfeeding time
• delayed development
• tantrums
• enuresis
• tics
• low birth weight
Clinical Characteristics
ADHD symptoms show different appearances at different ages. Most of the information obtained relates to primary school children. Smaller and larger data are scarce. However, parents state that even in infancy, the child moves left and right like an established motor. Some mothers even state that their children are very active even in the womb.
The main features of ADHD are difficulty in paying attention and sustaining attention, hyperactivity and agitation compared to children of similar developmental level.
“Attention deficit” is manifested by symptoms of difficulty concentrating on a subject, inability to complete assigned tasks, limited attention time, and distraction. Children with this disorder show a lack of attention to detail and make many mistakes in school and other homework. They continue their work in an unplanned, irregular and chaotic manner. They cannot concentrate for a long time in games and similar activities, and have difficulty completing the tasks they have started. They appear as if their minds are elsewhere or not listening or hearing what is being said.
They often move from one incomplete activity to another. They cannot be worked on the school assignment or any job assigned to them in a specified and expected manner; They cannot finish their homework. These children avoid work and tasks that require a certain mental effort (homework, writing, etc.) and are reluctant to take part in such activities. They cannot sit in a chair for long while doing their homework.
Even if they sit at the beginning of their classes for a while due to the force of their parents, they play with objects such as pencils, erasers and sharpeners. They can be easily distracted by irrelevant stimuli. A sound or an image that does not attract the attention of others immediately grabs their attention. The way they work is messy and unorganized. They often forget or lose their belongings and school supplies. They are often forgetful in daily activities. They do not listen to others, cannot concentrate on speaking, and cannot follow the rules of games or activities.
“Hyperactivity” is manifested in the style of being unable to sit comfortably or fidgeting even when sitting, not being able to sit still when necessary, running around in inappropriate environments or climbing on things, being constantly in motion “as if the engine is stuck”. These children act one after the other, without stopping, without heeding the warnings. Classroom teachers may complain that such children often stand up, taunt and talk to their friends. The phrase “straight wall climbing” is appropriate for these children, as they jump over seats and climb into lockers. They get into more dangerous and accident-prone situations than other children. Because they are very active and agile, they may not be able to grasp the danger immediately. They talk a lot and make noise during activities that require quiet.
“Impulsivity” is the impulsiveness that manifests itself by taking action without thinking about the consequences of a behavior. Impulsivity manifests itself in the form of impatience, the tendency to answer questions without completing them, difficulty in waiting their turn, interfering with others’ conversations or work.
Many challenges await these children when they start school. The child’s not sitting at his desk, his inability to concentrate on a subject, his perception disorder and clumsiness cause him to be constantly scolded, criticized and warned. In addition, the difficulties they experience in establishing and maintaining friendships can make them more introverted, lonely, angry, resentful and disruptive. This lays the groundwork for additional diagnoses such as oppositional defiant and conduct disorder.
These children have difficulty in organizing what they perceive. They often confuse the letters “b, d, p”. Because each of these can be another with various spins. This confusion also manifests itself in copying geometric patterns.
Another form of visual perception disorder is manifested by disruptions in location organization. These children often confuse left and right.
Depth perception problems are another aspect of visual perception disorders. Children with such problems estimate distances incorrectly, bump into objects. This is why parents often complain that their children are clumsy.
Fine motor coordination disorder is very evident in activities such as hammering nails, using cutlery, writing, and painting. A child’s hand never works as well or as fast as his thoughts. There are often two choices: either write very slowly and fail to finish assignments on time, or write quickly and make many mistakes. These children’s notebooks are irregular. Letter and syllable skipping, reversed letters and unfinished pages are the most distinctive features of notebooks.
Evaluation, Diagnosis and Differential Diagnosis
ADHD is a clinical diagnosis; There is no laboratory test or specific test to confirm the diagnosis. Clinician’s diagnostic tools are interviews with family and child, clinical observation, physical and neurological examination, behavioral assessment scales, and cognitive tests. It has been reported that quantitative EEG (Q-EEG) can be helpful in determining the attention deficit and hyperactivity subtypes of the disorder. In the evaluation, information is also collected from parents, teachers and other private individuals with the help of scales.
According to DSM-IV, 6 out of 9 symptoms on the hyperactivity-impulsivity list should be met for the diagnosis of hyperactivity and impulsivity, and 6 out of 9 symptoms on the inattention list should be met for the diagnosis of the type with marked attention deficit. In addition, the symptoms must begin before the age of 7 and the symptoms observed for diagnosis must be present in two environments such as home and school.
The most difficult differential diagnosis problem in the preschool period is distinguishing the mobility of normal children from those with ADHD. Many parents describe their children as careless and hyperactive. These complaints of children with true ADHD are chronic. These children always and everywhere engage in similar behavior.
Apart from attention deficit, different types of learning disorders that may occur due to inability in reading or math should also be differentiated from ADHD. Another important diagnosis that should be differentiated from ADHD is adjusment disorder. The duration of adjustment disorder is usually less than six months and the onset is later in life.
Anxiety disorders and depression can also cause hyperactivity and easy distraction. But anxiety and depression have their own specific symptoms.
Absence seizures should be considered in the differential diagnosis, as they may accompany ADHD or exhibit symptoms similar to ADHD.
Diagnostic Overlap (comorbidity)
Comorbidity (diagnostic overlap, comorbid disorder, or comorbidity) expressed as a child meeting the prescribed diagnostic criteria for at least one or more other disorders ADHD It is frequently observed in . ADHD is highly associated with oppositional defiant disorder (IDD) and conduct disorder (DD). It has been reported that children who do not have a family history of mental problems such as antisocial personality disorder, alcoholism or hysteria generally do not have behavioral problems, and children with such disorders in their families exhibit behavior problems as well as ADHD.
Comorbid disorders:
1. Conduct disorder (30-50%)
2. Oppositional disorder (50%)
3. Mental retardation
4. Autism
5. Tourette’s syndrome (20% of those with ADHD have tic disorder, and 40-60% of tic disorders have ADHD).
6. Fragil-X (73% of them have ADHD)
7. Learning disorders
Treatment
Psychosocial and medical interventions in the treatment of ADHD There are multi-modal approaches including:
• Medical treatment
• Parent education
• Cognitive-behavioral treatments
• Special education programs
• Diet regulation
Medication:
Two main groups of drugs are often used in the treatment of ADHD:
• Psychostimulants
• Antidepressants
Psychostimulants used in ADHD:
• Methylphenidate (Ritalin). It exists in Turkey.
• Dextroamphetamine (Dexedrine)
• Pemoline (Cylert)
• ADDERALL (methylphenidate and dextroamphetamine combination)
Antidepressants used in ADHD:
• Imipramine (Tofranil). It exists in Turkey.
• Desipramine (Norpramin)
• Buproprion (Wellbutrin)
Psychostimulants are the drugs most commonly used in the treatment of ADHD in the USA. Methylphenidate (MPH) is the most commonly used stimulant drug. Currently, only MPH is available in Turkey and can be prescribed with a controlled red line. Psychostimulants are also called non-catecholamine sympathomimetics. They act as direct (such as dopamine or norepinephrine) and indirect agonists on adrenergic receptors.
Psychostimulants reduce ADHD symptoms, cause dopamine release and block dopamine reuptake at presynaptic terminals. Binding of MPH is greatest in the striatum and is dependent on sodium concentration.
MPH is in tablet form and is rapidly absorbed after oral administration. Nutrients increase absorption. MPH easily crosses the blood-brain barrier. MPH is rapidly metabolized as it is not bound to plasma proteins and is not stored in adipose tissue. When the standard tablet is used, it reaches its peak value in plasma in 2 hours, and half of this value (half-life) in 3-4 hours. The effect of MPH begins 30 minutes after oral administration. It offers calm, normal and mature behavior at school with standard morning and afternoon doses. The recommended daily dose is 0.3-1 mg/kg.
Side effects of psychostimulants are related to positive adrenergic agonistic effects, as in adrenergic agonists. These side effects are insomnia, weight loss, decreased appetite, palpitations, drowsiness, headache, dysphoria, fear and vasomotor disorders. Most of these side effects are eliminated by reducing the dose of the drug for a short time. The side-effect known as “behavioral rebound” occurs in children who experience psychostimulant withdrawal at the end of the school day. In such children, evening irritability, babbling, non-adherence to treatment, excitability, hyperactivity and insomnia are detected 5-15 hours after the last dose. These behavioral symptoms are exaggerated versions of the main complaints. A slowdown in growth rates was seen in those using MPH for 2 years or longer. However, this has not been proven in some studies. After the second year, it was determined that tolerance to this slowing effect developed. Tolerance to MPH may occur, usually if the duration of treatment exceeds 1 year. This reduction in treatment response can be corrected by switching to another psychostimulant.
Specific dose adjustment: We should have height, weight, blood pressure, heart rate and complete blood count before the first drug is given. Although the effects of psychostimulants are close to each other, MPH should be the drug of first choice because of its high reliability.
MPH begins with a single 5 mg dose at 8:00 am for 3 days; an additional 5 mg dose is added at noon on the next 3 days; for the next 3 days, 10 mg is given at 8.00 in the morning and 5 mg at noon; Finally, the dose is increased to 10 mg in the morning and 10 mg in the afternoon and continued in the same way for at least 2 weeks. In order to keep the appetite suppressant effect at a minimum level, it is better to take it with or after a meal. Medication holidays (on weekends, during summer vacation or after school) are decided based on the child’s situation.
The average daily dose is 10-80 mg for MPH, 5-40 mg for dextroamphetamine, 20-60 mg for pemoline.
Approximately 25% of schoolchildren do not respond to psychostimulants. Tricyclic antidepressants (TSA) are used at least with MPH frequency in Turkey. In the TSA group, the most commonly used drug in Turkey is imipramine. ECG monitoring is required due to the risk of cardiotoxicity in the use of imipramine. The dose of imipramine in children is limited to 5mg/kg/day.
Cognitive-Behavioral Therapies:
As a result of treatment with this approach, more impulse control, longer thinking and proper motor activity are achieved.
When planning tasks for these children, what they need to do should be broken down into small pieces and made into steps. Also, additional time should be added for each step of the task. For example, 20 minutes of study and 10 minutes of break.
Parent Education:
In this education, it is aimed to inform the family about ADHD and attitudes towards the child. Burada anne ve babalara çocuklarına uygun disiplin ve tutarlı davranılması öğretilir. Aşırılı hoşgörülü veya aşırı cezalandırıcı tarzdaki yaklaşımlardan kaçınmalıdır.
Prognoz (Gidiş)
Geçmişte halk arasında ve tıbbi çevrelerde DEHB’nun yaş ilerledikçe kendiliğinden azalarak ergenlik döneminde iyileştiğine inanılırdı. Oysa son zamanlarda yapılan izlem çalışmalarında bunun doğru olmadığı, bu bozukluğun gidişinin farklı kişilerde farklı seyirler gösterdiği görülmüştür. Bozuklukta 3 ayrı gidişten söz edilmektedir:
1. Belirtilerin kaybolması: DEHB olan çocukların %30’unu oluşturur. Genç erişkinliğin erken döneminde belirtilerin kaybolduğu gruptur.
2. Belirtilerin sürmesi : DEHB olanların yaklaşık %40’ında gözlenir. Belirtiler çeşitli sosyal ve duygusal güçlüklerle erişkin dönemde de sürer.
3. Gelişimsel bozulma: DEHB olan %30 çocukta gözlenir. DEHB bulgularıın yanı sıra alkolizm, madde kullanımı ve antisosyal kişilik bozukluğu gibi psikopatolojilerin eklendiği gruptur. Bu kötü gidişin en güçlü belirleyicisi çocukluk döneminde DEHB’na komorbid olarak DB’nun binişikliği ve aile içi güçlüklerin ve olumsuzlukların olmasıdır.
Hiperaktivite yaşla birlikte azalmakta, ancak dikkatsizlik ve dürtü denetim sorunları kalıcı olabilmektedir. Genellikle ilk kaybolan aşırı hareketlilik, en son kaybolan ise dikkat eksikliğidir. Remisyonun 12 yaşından önce seyrek olduğu, genellikle 12 ile 20 yaşlar arasında görüldüğü bildirilmektedir. Ancak olguların önemli bir bölümünde bozukluk kısmi remisyona girmekte ve duygu-durum bozuklukları ile antisosyal ve diğer kişilik bozukluklarının ortaya çıkışı kolaylaşmaktadır. Öğrenme sorunları sıklıkla sürmektedir.
g. Uygulama: Yumuşak nörolojik belirtilerin öğrencilerle test edilmesi.
ğ. Özet: (3 Dakika)
DEHB aşırı hareketlilik, kısa dikkat süresi ve ataklıkla karakterize bir bozukluktur. Erkeklerde sık gözlenir. Karşı gelme bozukluğu, davranım bozukluğu ve öğrenme bozuklukları sıklıkla birlikte bulunur. Tedavide en etkin olan ilaç psikostimulanlardır.
Nükleus kaudatus, putamen, globus pallidus, nükleus subtalamikus ve substantia nigra oluşur. Bazal ganglionlarana fonksiyonu talamusdan geçenlifler aracılığıyla, motor korteksietkilemektir. Bazalganglionların amacı hareketin planlanması ve eşgüdüm halinde yapılmasıdır. Ayrıca bazal ganglionların duygulanım ve bilişsel fonksiyonlardanda sorumludur.
Nükleus
Nükleus kaudatus ve putamen’in beraber oluşturduğu yapıya striatum denir. Bazal ganglionlar motor merkezlerin fonksiyonlarına yardımcı olur. Bazal ganglionların girişi Striatum, çıkışı substansia nigra ve globus pallidustur.
Subtalamik nükleus lezyonunda ballismus olur. Tek taraflı olursa lezyonun karşı tarafından olur ve buna hemiballismus denir, irade dışı kasılmalardır.
Corpus striatum lezyonunda atetozis oluşur. Distoni ve Huntington koresi bu bölümle ilgili bozukluklardır. Huntington koresinde striatumdaki kolinerjik ve GABA erjik liflerde dejenerasyon vardır.
Substantia nigra lezyonları parkinsona neden olur. Substantia nigradan, striatuma dopaminerjik lifler gitmektedir. Parkinson hastalığında nigrostriatal yolda dejenerasyon vardır. Parkinson hastalığı rijidite, hipokinezi ve tremorla (hap yapar, para sayar tipi) karakterizedir.
NOT:
Trinukleotid Tekrar Sendromları
Fragil X:
Ailesel zeka geriliği,
karakteristik yüz görünümü(Uzun yüz, kepçe kulak),
konuşma ve davranış buzuklukları ile seyreder.
Globus Pallidus
The structure indicated is the globus pallidus.
The globus pallidus is a subcortical structure located within the cerebral hemispheres, and is a major component of the basal ganglia.
The basal ganglia are a group of subcortical nuclei (collection of neuronal cell bodies located within the CNS) located at the base of the forebrain. The term “basal ganglia” is a misnomer, and the name “basal nuclei” would be more appropriate, since ganglia are collections of neuronal cell bodies located within the peripheral nervous system. The basal ganglia form extensive connections with other areas of the brain and are involved mainly in the control of movement and posture.
The basal ganglia consist of the following main components:
Caudate nucleus
Putamen
Globus pallidus
Substantia nigra
Nucleus accumbens
Subthalamic nucleus
These components are grouped together as follows:
Caudate nucleus + putamen = striatum
Putamen + globus pallidus = lentiform nucleus
The globus pallidus lies medial to the putamen and consists of an internal (medial) and external (lateral) component, separated by the medial medullary lamina. The internal capsule runs medial to the lentiform nucleus. The posterior limb of the internal capsule separates the thalamus from the lentiform nucleus. The anterior limb of the internal capsule separates the putamen from the head of the caudate nucleus.
The globus pallidus is sometimes referred to as the pallidum, or the paleostriatum. The neostriatum is a term used to describe the caudate nucleus and putamen (striatum).
Learn more about the basic anatomy of the brain in this tutorial.
Beynin Lateral Yüzeyi
MSS beyin ve omurilikten meydana gelir. Beyin tamamen kafatası tarafından çevrelenmiştir. Aşağıdaki şekilde tipik bir insan beyni ve bütün memelilerde ortak olarak bulunan beyin, beyincik ve beyin sapı gözükmektedir.
Beyin (Serebrum) beynin en önde bulunan en büyük kısmıdır. Yukarıda ilk resimde de görebileceğimiz gibi beyin ortadan sağ ve sol olmak üzere iki kısma ayrılmıştır. Genel olarak sağ beyin/lob diye tabir edeceğimiz sağ kısım vücudun sol tarafından sinyal alıp yine bu tarafı kontrol ederken, sol beyin/lob da vücudun sağ tarafından sinyal alıp yine sağ tarafını kontrol eder. Yani biraz daha teknik konuşursak beyin çoğu zaman contralateral olarak çalışır.
Beyincik (Serabellum) hemen beynin altında bulunur. Buraya beyincik denmesinin sebebi gerçekten de ufak bir beyin gibi durmasındandır, burası da iki loba ayrılmıştır ve beyincikte nöron yoğunluğu fazladır. Beyincik birincil hareket kontrol merkezidir, beyin ve omurilik ile yoğun bağlantılar kurmuştur. Beynin aksine beyinciğin sağ lobu sağ vücudun hareketi ile ilgilenirken sol lobu da sol kısmın hareketi ile ilgilenir yani ipsilateral çalışır.
Beynin Dorsal Yüzeyi
İnsan beyninin dorsal bölümünün geniş serebrum kısmından oluştuğunu ve iki loba ayrıldığını demin görmüştük. Serebrumu kaldırırsak hemen altında yatan serebellumu yani beyinciği görürüz. Beyinciğin motor kontrolü için önemli bir bölge olduğunu söylemiştik demin. Beyinciğin orta kısmı Vermis yani orta lob olarak adlandırılıyor.
Serebrum ve serebellumu kaldırırsak beyin sapı açığa çıkar. Burada talamusun üzerinde bulunduğu epifiz bezi melatonin salgılar, uyku ve cinsel davranışı kontrol eder. Superior colliculus (colliculus latince tümsek demekmiş, superior da üst demek yani üst tümsekler diyebiliriz) gözlerden doğrudan bağlantı alır ve göz hareketlerini kontrol etme ile ilgilidir. İnferior (Alt) colliculus işitsel sistemin önemli bir parçasıdır. Beyincik sapı da serabellum ile beyin sapını bağlayan akson demetidir demiştik.
