Head Trauma

In approximately half of traumatic deaths, the cause of death is head trauma. In more than 60% of these patients, the etiologic factor is motor vehicle accidents. Because of the importance of head trauma, it is imperative that the physician who first sees the patient after trauma has adequate knowledge of the subject.

It is not always possible for a neurosurgeon to see a patient with central nervous system injury first. Therefore, one of the most important initial responsibilities of the general practitioner is to prevent changes such as respiratory disorders and hypovolemia that may lead to secondary brain damage.
The general practitioner should have the following basic information about a patient with head trauma when providing information to a neurosurgeon:

• Age of the patient and mechanism of injury
• State of the respiratory and cardiovascular systems
• Results of neurologic examination (especially level of consciousness, pupillary response to light, loss of limb motor power)
• Presence and type of injuries other than cerebral injuries
• Results of the examinations, if available

Neurosurgical consultation or referral to a more appropriate center should not be delayed for reasons such as obtaining computed brain tomography (CT) and direct radiography.

Anatomy and Physiology

A. Scalp: The scalp is a tissue composed of five layers covering the calvarium; (1) skin, (2) subcutaneous, (3) galea aponeurotica, (4) loose areolar tissue, (5) periosteum “pericranium”. Subgaleal hematoma is located in this anatomical localization. Tears in the scalp can cause significant blood loss, especially in children, due to the rich blood supply of this tissue.

B. Skull: It consists of a roof called the calvarium and a base called the basis. The calvarium is very thin, especially in the temporal region. The basal part is irregular and very solid. The brain can be injured by hitting the inner surface of the bone as it moves inside the skull during axialization and deselaration.

C. Meninges: The dura mater is a thick, fibrous membrane attached to the inner surface of the skull. Because the dura is not adherent to the arachnoid beneath it, there is a potential space in between called the subdural space. In certain places the dura splits to form the sinuses where the venous drainage structures of the brain drain. The superior sagittal sinus is the most vulnerable to injury because of its location.

Meningeal arteries are located in the epidural space between the inner surface of the skull and the dura. The grooves through which these arteries travel are visible on direct radiography. Since rupture of these arteries may result in epidural hematoma, a CT scan should be obtained in fractures crossing these grooves.

The second layer under the dura is a thin, transparent and vascular-free arachnoid. Below this lies the pia, which is well adherent to the cerebral cortex. Cerebrospinal fluid (CSF) circulates between the arachnoid and the pia. Bleeding into this space is called subarachnoid hemorrhage.

D. Brain: It consists of the cerebrum, cerebellum and brain stem. The cerebrum consists of the right and left cerebral hemispheres, separated by an extension of the dura called the falx. The left hemisphere usually contains the speech centers and is called the dominant hemisphere. The frontal lobe is involved in behavior and motor function, the occipital lobe in vision and the parietal lobe in sensory function. The temporal lobe regulates some memory functions.

The brain can be compared to a funnel. The two cerebral hemispheres form the upper part of the funnel and the brain stem, through which important neural information pathways pass, forms the neck. The midbrain and the upper part of the pons contain the reticular activating system that maintains the waking state. Vital cardiorespiratory centers are located in the medulla in the lower part of the brainstem. The cerebellum surrounding the pons and medulla in the posterior pit is responsible for coordination of movements, regulation of tone and balance.

E. Cerebrospinal fluid (CSF): It is produced by the choroid plexuses and released into the brain ventricles. This fluid leaves the ventricular system and enters the subarachnoidal space.

F. Tentorium: This structure divides the intracranial cavity into two cavities, supratentorial and infratentorial. The midbrain extends downward through the large opening (incisura) in the tentorium. The cranial nerve III (oculomotor nerve) also passes through this opening. As a result of pathologic changes such as hemorrhage, edema, etc. that rapidly increase supratentorial pressure, the medial part of the temporal lobe is pushed towards this opening. As a result of unkal or tentorial herniation, the oculomotor nerve is compressed and a dilated fixed pupil appears on the same side. Spastic loss of strength in the opposite half of the body is the result of compression of the cortico-spinal fibers in the cerebral peduncle for the same reason.

G. Consciousness: The level of consciousness is one of the most important signs of the severity of trauma in brain injury. Bilateral injury to the cerebral cortex and injury to the reticular activating system in the brain stem can cause loss of consciousness. Increased intracranial pressure and decreased cerebral blood flow may cause disturbances in the level of consciousness without any other cause.

H. Intracranial pressure: It can be defined as the relationship between the volumes of CSF, blood and neural tissue filling the intracranial cavity. This relationship can be expressed by the Monroe-Kellie equation.

Due to the mass effect caused by hematoma or cerebral edema, CSF or venous blood (sometimes both together) escapes from the intracranial cavity in larger amounts than normal. Due to these changes, which aim to keep the intracranial volume constant, a volume of 50-100 ml can be compensated, depending on the location of the mass and the rate of expansion. When the normal compensatory reserve is depleted, even small changes in intracranial volume will cause a decrease in cerebral perfusion pressure, resulting in a significant increase in intracranial pressure.

Cerebral perfusion pressure is obtained by subtracting the intracranial pressure from the mean systemic arterial pressure. This is the arterial perfusion value of brain tissue and is normally greater than 50 mm Hg. In the first moments of elevated intracranial pressure, systemic arterial pressure also rises to maintain cerebral perfusion. However, when intracranial pressure continues to rise, cerebral perfusion pressure begins to fall. As a result, ischemia develops, which can lead to changes in the level of consciousness. In cases where intracranial pressure is higher than systemic arterial pressure, cerebral blood flow is blocked and brain death develops.

One of the most important conditions in the management of increased intracranial pressure is the continuous direct measurement of arterial, central venous and intracranial pressures.

III. Evaluation of Head Trauma

A. Story

In order to make the right decision regarding management, it is necessary to know what type of head trauma the patient has suffered. The cause of the trauma is often obvious, but even if the patient has a good neurologic status, the risk factors for injury must be well evaluated in order to decide how and where to treat the patient. For example, it should be known that one in four patients may develop an intracranial hematoma as a result of a fall.

It is very important that the information to be obtained from the people who saw the patient at the scene of the accident and ambulance personnel is recorded in detail and transmitted to the emergency physician. 

B. Initial assessment 

The importance of the initial assessment should be emphasized. Because it will form the basis for many critical decisions regarding the patient's management. 

Providing an adequate airway and stabilizing respiratory and circulatory functions should be the priority. It should be kept in mind that a systolic blood pressure of less than 60 mm Hg or the presence of systemic hypoxemia may cause changes in the patient's mental status. It should also be considered that alcohol or other nervous system depressants may have been ingested. 

C. Detection of vital signs 

Although brain injury can cause changes in vital signs, it is not easy to determine whether these changes are due to head injury or other factors. Some useful clinical guidelines in this regard are as follows:

1. Cerebral injury should never be considered as a cause of hypotension. Although hemorrhage from scalp injury can sometimes cause hemorrhagic shock, especially in young children, intracranial hemorrhage alone often cannot do so. Hypotension as a result of brain injury is a terminal development due to insufficiency of medullary centers.

2. The specific response to a sudden and fatal increase in intracranial pressure is bradycardia, progressive hypertension and respiratory failure (Cushing's triad).

3. Hypertension alone or in combination with hyperthermia is a consequence of central autonomic dysfunction seen in some brain injuries.

D. Brief neurological examination

A brief neurologic examination should be performed in every patient with head trauma. As a result of the examination (1) level of consciousness, (2) pupillary functions, (3) lateralization can be detected immediately. Detection of these changes usually indicates a pathology that requires surgical intervention. 

Level of consciousness

a. Glasgow coma scale

It provides a quantitative assessment of the patient's level of consciousness. The total score obtained with the scores given in the three sections gives fairly accurate information about the clinical picture.

1) Eye opening response (E): This assessment is not performed when the eye is closed due to edema or hematoma. 

2) Verbal response (V): Not possible to assess in intubated patients.

3) Motor response (M): Refers to the best motor response from any extremity. During the evaluation, the painful stimulus can be applied to one of the fingernails or toenails.

b. Classification of patients

The Glasgow coma scale (GCS) can also be used for this purpose.
Coma; GCS score is between 3-8 or in other words, a score of 8 or below. A score between 9-12 indicates moderate head trauma, and a score between 13-15 indicates mild head trauma.

Pupil examination

The pupils are evaluated for their equal size and their response to light. A difference of more than 1 mm in both pupil diameters is interpreted in favor of abnormality.

Motor weakness

Spontaneous movements are observed for equality. If there is no spontaneous movement or very little, painful stimulus can be applied. Delay in the onset of movement on one side, decrease in mobility or application of more severe painful stimulus are considered significant.

IV. Purposes of Neurological Examination

The purpose of the brief neurologic examination is to determine the severity of the brain injury and to detect early deterioration in the neurologic picture. The presence of any of the following should suggest severe head trauma:

a. anisocoria
b. lateralization
c. CSF fistula or injuries with brain tissue outside
d. neurologic deterioration
e. depressed fractures

A decrease of two points or more in the GCS score indicates deterioration in the patient. A decrease of three points or more in the score indicates fatal deterioration and urgent surgical intervention is necessary if the cause is determined. In some cases, neurologic deterioration is determined by the following changes:

f. Increased headache or unusually severe headache
g. Enlargement of one pupil
h. Occurrence of hemiparesis

It should be remembered that the initial neurologic examination is only a preliminary one. The findings detected at the beginning will form the basis for subsequent neurologic examinations.

V. Diagnostic Methods

A. Direct head radiographs

Except for penetrating injuries, they do not provide information that greatly affects the early management of patients with head trauma. In an unconscious patient, head radiographs may be allowed only after vital functions have stabilized. Physical and systemic examinations are generally more valuable than direct head radiographs. In skull base fractures in particular, it is more useful to identify clinical findings than to attempt to see these fractures on direct radiographs. There is an increasing tendency not to obtain direct radiographs in cases with mild head trauma.

B. Computerized brain tomography

It is a method that has revolutionized the field of diagnosis in cases with head trauma. It is the diagnostic method that should be selected in cases with severe head trauma or suspected severe head trauma. 78 Although not perfect, CCT shows the exact location and size of most lesions. CCT has replaced less specific and more invasive methods such as cerebral angiography.

CCT should be obtained at an appropriate time in all cases except mild head trauma. In more severe injuries, the need for CCT is earlier and more urgent.

If the patient is found to need a CT scan after the initial intervention, (1) resuscitation should be continued during the scan and (2) the highest quality, adequate scan should be performed. Movement of the patient during the scan will cause artifacts and inadequate filming. These artifacts may mask lesions requiring urgent surgical intervention. Movement artifacts can be prevented by using sedatives in uncooperative patients. However, in this case, the patient should be closely monitored for hypoxia. In some cases where CT is essential, the patient is intubated and controlled respiration is applied. In this way, movements can be prevented with respiratory paralysis drugs. The consultant physician must evaluate the patient before anesthesia or CT is performed.

C. Other tests

Tests such as lumbar puncture, EEG, isotope imaging have no place in emergency management of head trauma.

Types of head trauma

After the initial evaluation and resuscitation, emergency management of a head trauma case should aim to (1) identify anatomical diagnostic features, (2) meet the metabolic needs of the brain, and (3) prevent secondary brain damage due to treatable causes such as increased intracranial pressure.

Head traumas include (1) skull fractures, (2) diffuse brain injury, and (3) focal injuries. The pathophysiology, vitality, need for emergency surgical intervention, and exit characteristics of each group are different from each other.

Skull fractures

Although skull fractures are quite common, they are often not associated with serious brain injury. Conversely, skull fractures may not be present in injuries resulting in serious brain damage. A detected fracture should suggest a developing or potential bleeding, and the patient should be hospitalized.

1. Linear fractures; They are seen as a line on direct radiographs. They may be star-shaped. No treatment is required for simple fractures. Fractures that cross vascular grooves and suture lines should be treated more carefully because they carry the risk of epidural hematoma.

2. Compression fractures; In some cases, they are urgent in terms of neurosurgery. Treatment is directly aimed at the underlying brain injury. Bone fragments that have collapsed more than the skull thickness should be surgically removed in order to reduce a possible risk such as epilepsy.

3. Open compression fractures; This condition is easily diagnosed if there is neural tissue or CSF leakage from the wound. Bone fragments should be surgically removed and the dura should be closed to reduce the risk of infection.

4. Skull base fractures; These fractures are often not seen on direct radiographs. Indirect air or opaque sphenoid sinus can be seen in the skull. Diagnosis is based on physical findings such as CSF fistula from the nose (rhinorrhea) or ear (otorrhea). If the CSF is mixed with blood, it may be difficult to decide. If a drop of this liquid is dropped onto a tissue or filter paper, the blood will remain in the center and the increasingly clean CSF will expand in rings around each other.

Findings such as ecchymosis on the mastoid (Battle sign) and blood behind the tympanic membrane (hemo tympanum) indicate a mid-base fracture. Cribriform plate fractures are usually accompanied by bilateral periorbital ecchymosis (raccoon eyes). These findings can sometimes take hours to appear. In frontal base fractures, care should be taken to ensure that the nasogastric tube is not accidentally inserted into the intracranial cavity.

VI. Diffuse Brain Injury

Diffuse brain injury occurs when rapid head movements (acceleration and deceleration) cause widespread cessation of function in a large part of the brain. As in concussion, this neural dysfunction is temporary. However, in more serious injuries (diffuse axonal injury), microscopic changes seen throughout the brain structure are the reason for the permanent damage.

1. Concussion; There is a short-term loss of neurological function. In milder forms, there is only a short-term confusion or amnesia. More often, concussion can cause a short-term loss of consciousness. Most patients with concussion are awake or have woken up in the emergency room. They can relatively remember the accident after a while. They may complain of headache, dizziness or nausea. Neurological examination may not show any localizing findings. These patients should be monitored and sent home after they regain full consciousness. As a rule, in cases of loss of consciousness lasting longer than five minutes, the patient should be kept under observation for 24 hours.

2. Diffuse axonal injury (DAI); It is often used to describe severe blunt head trauma, diffuse trauma and brainstem injuries. It is accompanied by a prolonged horn state that can last from a few days to a few weeks. The mortality rate is 33%. In severe forms, this rate increases to 50% due to changes that lead to cerebral ischemia. DAI is primarily microscopic changes that are widespread throughout the brain. Therefore, surgical treatment is not possible. The diagnosis should be confirmed with an early CBT examination, often performed in patients with decorticated or decerebrate posture. DAI can be divided into three degrees; (1) axonal injury is in the white matter of the cerebral hemispheres, corpus callosum, brainstem and cerebellum (2) in addition there is a focal lesion in the corpus callosum (3) in addition there is a focal lesion in the dorso-lateral part of the rostral part of the brainstem. High fever, hypertension and sweating caused by autonomic dysfunction are common. The patient should be referred to a resuscitation clinic where long-term coma treatment can be provided as soon as possible.

VII. Focal Injuries

It refers to macroscopic damage seen in a relatively smaller area. The most important goal in the early post-traumatic period is to be able to reveal these lesions, which can be treated surgically, without delay.

1. Contusion; They can be single or multiple, and they can be small or spread over a large area. Contusions are often found together with serious concussions that cause long-term coma or mental confusion. They can be just below the impacted area (coupe lesions) or on the opposite side (contrecoupe). They are most commonly seen in the end parts of the frontal or temporal lobes. Contusions close to the sensory and motor cortices of the brain can cause focal neurological deficits, while some may remain silent. If the contusion is very large or accompanied by widespread edema in the surrounding tissue, it causes herniation or secondary brain damage due to brainstem compression and late neurological impairment.

Patients suspected of cerebral contusion should be hospitalized. If there is a life-threatening mass effect, surgical intervention may be required. Caution should be exercised in patients who have consumed alcohol, as the risk of bleeding into the contusion is higher.

2. Intracranial hemorrhages; It is possible to divide them into two main groups: meningeal and parenchymal hemorrhages.

a. Meningeal hemorrhage

Acute epidural hemorrhages: Epidural hemorrhages almost always occur as a result of rupture of the dural arteries, usually the middle meningeal artery. A very small portion may occur as a result of rupture of the dural sinuses. Epidural hemorrhages are seen in 0.5% of blunt head traumas and 0.9% in comatose cases. Although they have extremely promising results if diagnosed and operated on early, they result in death if delayed. They are especially associated with fractures that cross the vascular grooves in the temporal and parietal bones.

The typical clinical development of epidural hematoma can be summarized as follows; (1) short-term loss of consciousness immediately after the trauma, (2) a period of full consciousness -lucid interval-, (3) loss of consciousness again, (4) hemiparesis on the opposite side. If the patient is caught in the intermediate period, he may complain of severe, localized headache.

Emergency surgical intervention should be performed without delay. If treated early, the prognosis is excellent. The postoperative clinical picture is directly dependent on the preoperative picture. The mortality rate in patients who are not in a coma is 0%. In the case of semicoma, this rate increases to 9% and in the case of severe coma, to 20%. If the evacuation of the hematoma is delayed, the consequences of secondary brain damage will also be added to the picture.

Acute subdural hematoma: They are more common than epidural hematomas. This rate is 30% in severe head traumas. They mostly occur as a result of rupture of the bridging veins between the cerebral cortex and the dura. However, some of them may be accompanied by laceration in the neural tissue. In addition to the mass effect of the blood in the subdural space, the primary brain injury is also serious. The prognosis is quite poor, with a mortality rate of around 60%. There are studies reporting good results in patients in whom the hematoma is drained very early.

Subarachnoidal hemorrhage: The CSF is perfused and meningeal irritation occurs. There is no place for emergency surgical intervention. Since the diagnosis is often made with CBT, there is no need for lumbar puncture.

b. Brain hemorrhages and lacerations

Intracerebral hematomas: They can be seen in any localization. They are diagnosed with CBT. Very small, deep intracerebral hemorrhages are associated with other types of brain injuries such as DAY. Neurological deficits may vary depending on the location, size and continuation of bleeding of these accompanying injuries. Hemiplegia may be observed. Occipital hemorrhages may cause visual field defects. Intraventricular and cerebellar hemorrhages are associated with a high mortality rate.

Injuries with sharp objects: Sharp objects thought to have entered the skull should not be touched until the patient is taken to surgery by a neurosurgeon. Skull radiographs may be helpful in obtaining information about the depth and angle of the object.
Gunshot wounds: Large-caliber and high-penetration bullets are more likely to kill. Patients with an entry GCS score of less than six have a higher mortality rate. Antiseptic moistened pads should be applied over the entry and exit wounds until the patient is taken to surgery.

Time factor; Early detection and evacuation of the hematoma will positively affect the prognosis. Epidural hematomas are often of arterial origin. Therefore, they grow faster. While 4-6 hours is sufficient for these hematomas to become clinically apparent, this period is 12-24 hours for subdural hematomas, which are more often of venous origin. Therefore, the decision to refer patients on time is as important as surgery.

VIII. Emergency Response to Head Trauma

Establishing a diagnosis

Evaluating the need for surgery: Three basic factors should be considered in estimating the potential need for emergency surgery in a patient; (1) the presence of a coma, (2) whether the trauma was caused by a motor vehicle accident, (3) whether there is a lateralized motor deficit.

Diagnostic system; A simple and systematic clinical assessment summary can be created based on a brief neurological examination. However, it should be remembered that this is only a guide. It is not possible to create a complete summary due to the complexity of brain injuries and the fact that they often do not occur alone.

First of all, it is necessary to determine the level of consciousness. GKS is used for this purpose. In cases where the score is 8 or less, the doctor should first check whether the pupils are equal and whether there is a lateralized motor deficit. If these are detected, one of the pathologies requiring emergency surgery should be considered and the necessary planning should be made immediately.

Although it is not possible to rule out a pathology requiring surgery in patients with coma with equal pupil size and motor responses, diffuse axonal injury, acute brain swelling or cerebral ischemia are often present.

Emergency intervention

Once a diagnosis is made, treatment should also be planned immediately. The urgency of treatment depends on the nature and severity of the injury. In seriously injured patients, brain tissue can be protected from secondary consequences by ensuring adequate cerebral metabolism and preventing and treating intracranial hypertension.
Adequate maintenance of cerebral metabolism; Cerebral ischemia or hypoxia causes insufficient material to be sent to the damaged brain tissue. These changes, which lead to a vegetative state or death, are largely preventable complications.

The brain's basic metabolic resources are oxygen and glucose. These are consumed at high rates. Since the metabolic rate in injured brain tissue also decreases, the need for oxygen and glucose decreases. The damaged tissue has become more sensitive to a new trauma due to the insufficiency of these substances. All these changes can only be prevented by having sufficient levels of these substances in the blood. Hyperglycemia should be avoided while this is being achieved.

The amount of oxygen depends on arterial hemoglobin and oxygen density. Arterial oxygen saturation can be determined by blood gas tests and, if necessary, oxygen should be administered to ensure that the P02 pressure is kept above 80 mmHg. Blood transfusion may be required to increase normal oxygen carrying capacity.

Cerebral blood flow depends on systemic arterial pressure and PCO2, especially immediately after head trauma. Normalization of blood pressure and keeping the PaCO2 level between 26-28 mmHg is often sufficient. In order not to increase intracranial pressure further, the PaCO2 level should not be allowed to increase too much.

Prevention/treatment of intracranial high pressure; The aim of this treatment is to prevent, control or reduce increased intracranial pressure regardless of the cause. In addition, space-occupying lesions, acute brain swelling (vascular dilation) and brain edema trigger intracranial hypertension.

a. Creating hypocapnia; Arterial carbon dioxide greatly affects cerebral circulation. When it increases abnormally, there is expansion in the cerebral vessels, in which case intracranial blood volume and pressure increase. Conversely, if its amount decreases, blood volume and therefore intracranial pressure will also decrease. Hyperventilation decreases intracerebral acidosis and increases cerebral metabolism. Therefore, hyperventilation is recommended so that PCO2 is 26-28 mm Hg. This procedure can usually be done with endotracheal intubation, controlled breathing and intermittent respiratory paralysis.

b. Fluid control; Fluid should be administered intravenously in a controlled amount that will not cause cerebral edema. The content and amount of fluids may vary depending on the patient's systemic condition. Continuous fluid administration should not be hypoosmolar.

c. Diuretics; Diuretics such as mannitol cause excessive urine output as a result of intravascular hyperosmolarity. It is very effective in reducing normal brain volume and lowering intracranial pressure. It should definitely be used under the supervision of a neurosurgeon in patients with worsening neurological status or a lesion requiring urgent surgical intervention in the emergency department, and in patients who want to gain time until surgery. The dose is 1 g/kg. It should be given intravenously and in bolus form.

The neurosurgeon may recommend diuretics such as furosemide (40-80 MGK IV for adults). A catheter should be inserted in these patients to monitor urine volume.

Isotonic fluids should be given to patients whose blood pressure drops rapidly during the use of these drugs.

d. Steroids; It has no place in acute head traumas.

Some rare problems in head traumas

Epilepsy

Focal or generalized seizures can occur with any type of injury. They can occur during or immediately after a sudden injury and often do not tend to become chronic. If it is a single seizure, no treatment is required. If the seizure duration is prolonged or if multiple seizures occur one after another, rapid and effective treatment is necessary as it will cause cerebral hypoxia. The most commonly used first-line treatment option is 10 mg diazepam given intravenously. Changes in respiration should be closely monitored: if the patient tolerates this dose, it can be repeated. Phenytoin (1 g iv, 50 mg/hour) should be started as soon as possible. The patient's blood pressure and ECG should be closely monitored. If seizures continue despite diazepam and phenytoin, phenobarbital or an anesthetic should be given.

Restlessness

It is often associated with brain injury and/or cerebral hypoxia. It may be the first sign of a space-occupying lesion developing in a previously quiet patient. In such a case, all attention should be directed to the possibility of cerebral hypoxia and its etiology. 84 Pain, bladder distension, tight bandages, plaster casts or systemic hypoxia may cause restlessness. When these etiological factors are controlled, restlessness and constant movement are also treated.

Intravenous morphine compounds given for pain treatment are not given until neurosurgical consultation, as they may cause respiratory depression or mask the neurological picture. However, if the patient has undergone a BCT examination, chlorpromazine (10-25 mg, iv) may be useful for severe agitation. This drug should be given with caution, as it may cause hypotension.

Hyperthermia

It is a development that worsens the situation in the injured patient. The increase in body temperature will increase the carbon dioxide level and the brain metabolic rate. The patient's fever is tried to be reduced by applying cold compresses. Chlorpromazine can be used to prevent shivering.

Scalp injuries

Despite their dramatic appearance, scalp injuries are very well tolerated and usually do not lead to very serious complications.

Blood loss

They can cause significant blood loss, especially in children. If the adult patient is in shock, scalp injury is usually not the only cause. The general approach principle is to find the cause of bleeding and stop it. If the bleeding is from relatively large arteries such as the superficial temporal artery, it should be held with a hemostat and tied. In cases of bleeding resulting from deep scalp laceration, control is often achieved by pressing on it for a few minutes.

Wound inspection

The wound should be carefully checked for foreign bodies and skull fractures. Inspection without seeing with a finger or an instrument should be avoided. It should be checked with inspection whether there is an EMPTY coming from the wound.

Suturing the scalp

The first step is to thoroughly irrigate the scalp with physiological serum. Skin pieces and hairs should be removed. Bone pieces should not be touched. Because they may be buffering a bleeding. In case of any doubt, neurosurgery consultation should be made. After the area around the scalp is shaved, the galea is first sutured. Then, stitches are placed on the skin and the head is wrapped with an elastic bandage or gauze to create light pressure.

Organic Brain Syndrome (Head Trauma)

Mild Traumatic Brain Injuries

Organic Brain Syndrome is a name given to a person who has suffered a mild closed brain injury and has a series of symptoms such as mood and anger problems, concentration difficulties, headaches and fatigue that last for years or even a lifetime.

Organic Brain Syndrome

When the head receives a hard blow, the difference in motion between the brain and the skull is severe, resulting in a traumatic brain injury (TBI). Although the maximum damage occurs at the moment of impact, the frontal and temporal regions are constantly susceptible to bruising and contusions regardless of the point of impact. In addition to the damage at the moment of impact, there is also damage caused by the brain hitting the skull and bouncing back, which can cause a problem later. The disruption of the boundary between white and gray matter can cause axonal breaks.

The term Organic Brain Syndrome, or the term concussion disorders as expressed in the DSM-IV, is defined in terms of the classification of residual symptoms (residual symptoms) that persist for 12 months and sometimes years after the injury. Although mild head injuries are considered harmless, a significant number of people report symptoms that persist for weeks, months, and sometimes years after the injury, even if no abnormalities are seen on MRI and CT scans. The core of the problems in Organic Brain Syndrome are Attention Deficit, Adaptation Difficulty, and Mood Disorders. In addition, those who suffer from these problems often report problems with memory and socialization, frequent headaches, and personality changes. A group of symptoms reported by patients indicate Organic Brain Syndrome. The following are the most commonly reported symptoms of organic brain syndrome.

• Attention Deficit, difficulty maintaining mental strength.
• Fatigue, exhaustion
• Impulsivity, irritability
• Easily frustrated
• Mood outbursts and mood swings
• Learning and memory problems
• Impaired planning and problem solving
• Stubbornness, fixed thinking
• Lack of initiative
• Disruption between thought and action
• Difficulty communicating
• Socially inappropriate behavior
• Lack of insight and “me” focus
• Problems with self-awareness
• Impaired balance
• Dizziness and headaches
• Personality changes

Despite these chronic symptoms, there may be no evidence of abnormalities in the brain on commonly used classical imaging tests such as CT scans and MRIs. As a result, this person may be classified as “angry, easily angered” or as having mood and/or anger problems, or as having a personality disorder or psychological problem.

The findings have an organic basis.

The fact is that these complaints seem to contradict the “negative” medical findings and create a debate about whether the organic brain syndrome is organic or psychologically based. However, over the past 30 years, evidence has been accumulated for the organic (brain-based) etiology of the organic brain syndrome, including cerebral blood flow, neuropsychological disorders, evoked potential recordings, PET, SPECT, MRI and QEEG. The nature of the head injury has been widely debated and theoretical concepts have been formulated that are supported by QEEG evidence.
Scientific literature states that Organic Brain Syndrome (Head Trauma) can be determined with very high specificity with the QEEG-Data Bank and that Neurotherapy is also an extremely effective treatment.

Assessment of Organic Brain Syndrome

The tests described below compare scores statistically with a very large database of people who have no disease. These tests have been validated in published and peer-reviewed scientific studies and are suitable for use in diagnostic systems. Together, they provide convergent evidence that organic brain syndrome has an organic basis, which is possible with specific treatment, Neurotherapy.

Quantitative EEG (QEEG)

QEEG is a statistical assessment of electrical activity in the brain. It is particularly suitable for the assessment of Organic Brain Syndrome because it has been shown empirically, objectively, and with high sensitivity to diagnose and differentiate various neurophysiological patterns of brain dysfunction associated with mild traumatic brain injury and organic brain syndrome (head trauma). A review of recently published scientific literature studies confirms that QEEG is much more successful than other visual techniques in detecting brain dysfunction associated with mild traumatic brain injury and organic brain syndrome (head trauma).

Mild Traumatic Brain Injury (MBI) Discriminant Analysis

The Brain Injury Probability Index tells you with statistical probability whether a person has mild traumatic brain injury. It also provides additional evidence supporting the conclusion that the symptoms associated with organic brain syndrome are organic. More than 34,000 studies have been published on QEEG since 1990. No negative results have been obtained in these studies. The only negative critical area of ​​research regarding the clinical use of QEEG was published by Newer of the Academy of Neurology in 1997. The ideas expressed in that study were discredited and refuted without a thorough review by the Association for Clinical EEG and Clinical Neuroscience as vague, based only on suspicion and lacking supporting evidence. Since then, the QEEG Neuroguide system has also been approved by the FDA for its use in the diagnosis of organic brain syndrome.

Attention Variables Test (T.O.V.A)

Attention Variables Test (T.O.V.A) is a continuous performance test conducted via computer. It is a test in which test participants are asked to press the button in their hands when they see the target on the computer and to hold themselves when they do not see the target. Scores are compared according to the appropriate age in order to obtain standardized scores and provide useful and objective information according to the four variables of attention.

* Attention and concentration and maintaining mental effort
* Impulse control
* Reaction time
* Displacement of attention (variability in responses)

T.O.V.A is an objective, stand-alone and empirical measurement that measures the degree of deterioration in the attention system.

Organic Brain Syndrome (Head Trauma) Treatment

A study in the October 2004 issue of Clinical EEG and Neuroscience concluded that QEEG is the most sensitive visual tool for assessing organic brain syndrome and that neurotherapy is the most promising treatment for organic brain syndrome.

Medication, Counseling, and Cognitive Therapy

Medication may temporarily help with distress, and counseling may help some people understand impulse and anger control. However, there is no evidence in the literature that medication or cognitive therapy effectively improves cognitive problems or concentration in organic brain syndrome.

Neurotherapy

People with attention problems and mild traumatic brain injury have more slow brain wave activity and coherence abnormalities. Neurotherapy (EEG Biofeedback) operant conditioning method gives patients visual/auditory rewards to produce more normal patterns in brain wave activity. Studies since the 1970s have shown that with neurotherapy, patients can learn to normalize dysfunctional brain wave patterns and help develop normal function in their brains. The latest development in neurotherapy is the ability to identify specific brain wave patterns that need correction using QEEG.

Neurotherapy can also be used to increase mental performance and improve concentration in people without organic brain syndromes