Central Nervous System Traumas

Severe central nervous system traumas occur in most of the traffic accidents, which are quite common in our country. In many countries of the world, trauma is one of the leading causes of death and disabilities in children, adolescents and young adults.  Severe injuries of the brain, spinal cord and of their supporting structures may occur as a result of motor vehicle crashes, falls and impacts which account for the majority of accidents.

Head Trauma

Scalp Injury:

If a scalp injury is not treated immediately, it may cause bleeding and subsequent shock.  Bleeding can usually be controlled by compression dressing or placement of clamp on the scalp.  The laceration of the scalp should be closed up as soon as possible.  Scalp lacerations covering collapse fractures or penetrating skull injuries should be sterilized and closed up in the operating room environment.  Simple scalp lacerations should be sterilized, irrigated plentifully and closed up primarily by taking care of approaching the layers of the galea and skin.  If the galeal layer is closed up well, an excellent bleeding control is achieved.  Scalp avulsions typically include all other layers except the periosteum.  If an avulsion is inconsiderably, closing the wound edges up primarily usually results in success.  In cases of large scalp avulsions, suturing the ruptured part by microsurgical technique is the preferred technique if the ruptured tissues are stored properly and the surgery is not delayed.

The defects can be repaired with grafts in cases in which the injured scalp loses its vitality but the periosteal layer is intact. In such cases, the periosteum should be kept moist before the surgery.  Since tabula externa provides the blood supply via periosteal layer, the repair is more difficult in case the periosteum does not exist or is dissected. Any type of scalp laceration needs to be evaluated by a neurosurgeon.

Skull Fractures

Skull fractures are classified according to the intact skin on the facture (closed fracture) or lacerated skin (open or compound fracture), a single fracture line (linear fracture), the presence of a multiple fracture lines from one focus (stellate fracture) or segmental fracture (comminuted fracture) and/or collapse of fracture line edges below the level of intact bones (collapsed-depressed fracture) or non-collapsed fracture (non-depressed fracture).

Simple skull fractures (linear, stellate or segmental non-depressed) do not require any special treatment.  However, they cause a potential danger if they cross vascular channels in the skull such as the arteria meningia media or dural venous sinuses. If these structures are torn, an epidural or subdural hematoma may occur.  Simple skull fractures that extend to nasal sinuses or mastoid air cells due to the contact with air are defined as "open fractures".

Collapse fractures often require surgical intervention to elevate bone fragments displaced inwards.  If there is no neurological finding and the fracture is closed, surgery may be performed under elective conditions.  The dura should be examined and repaired during surgery if necessary.

Open skull fractures also require surgical intervention. Linear or stellate non-depressed open fractures can be treated by simply closing after they are completely cleaned.  Compound open fractures with severe injury of below bone should be repaired in the operating room environment where an effective debridement can be performed.  The dura should be examined carefully for not to miss dural tears. Dural tears should be closed up primarily or with fascia grafts to reduce risk of infection and prevent CSF leak.  Considering the requisite to visualize the below dura and/or the brain tissue better, open collapse fractures should be cleaned and removed in the operating room once the preparations for craniotomy have been completed.

Bruising around the eyes (raccoon eyes sign) or behind the ear (battle's sign) may be seen in basilar skull fractures.  These clinical signs are more common in the anterior and middle fossa fractures.  In such fractures, isolated cranial nerve lesions may be seen as the holes (foramina) of the cranial nerves are localized on the base of the skull.  The facial nerve is the most common nerve affected by basilar skull fractures due to laceration or oedema.  Majority of facial nerve lesions heal spontaneously and do not require any treatment.  On the other hand, complete lacerations of the facial nerve are usually explored surgically, but the timing of the surgery is controversial.

The cases accompanied by rhinorrhea or otorrhea, in other words cerebrospinal fluid leaks from the nose and ear, are expected to be treated.  Traumatic CSF leaks typically stop within the first 7 to 10 days.  However, this treatment should be absolutely carried out under the supervision in a neurosurgery clinic.

Cerebral Laceration (crushing):

Brain laceration occurs due to deceleration, acceleration, rotation, or their combination as a result of an impact on the head.  During the first impact, neuronal and axonal tears may develop which causes the primary damage.  Any subsequent complications such as intracranial hematomas, brain oedema, hypoxia, hypotension, hydrocephalus or endocrine disorders cause the secondary damage.

Mild head trauma is usually not accompanied by primary brain injury and usually neurological deficits are limited to transient loss of consciousness (concussion).  On the other hand, typically reversible or irreversible neurological deficits may be seen in moderate and severe head traumas.  Moreover, a secondary trauma usually accompanies a trauma at this level.

Intraparenchymal capillaries causing the primary injury may be as severe as to tear superficial subdural bridge veins or epidural arteries and veins and consequently hematomas may occur as extravasation.  Brain oedema may bee seen as a result of vasodilatation and deterioration of the blood-brain barrier. Ischemia occurred due to hypotension and hypoxia may cause cell death and cytotoxic oedema. Blood-contaminated CSF may result in impaired CSF absorption and hydrocephalus.  The release of inappropriate antidiuretic hormone or diabetes insipidus may further exacerbate cerebral oedema by impairing the fluid and electrolyte balance.  Separately or together, these changes may result in ICP elevation.

The elevated ICP plays a role in the secondary brain injury by decreasing the cerebral perfusion pressure (CPP).

Intracranial hypertension is one of the most important factors that affects the prognosis in head traumas.  Therefore, when the cerebral perfusion pressure reduces, aggressive treatment is mandatory to be administered to prevent the secondary injuries in the brain.  If possible, early intervention should be performed in the accident area using airway control and hyperventilation.

A rapid clinical evaluation is essential.  Although a thorough neurological assessment is difficult in non-responsive and uncooperative patients, some certain characteristics are of critical importance in trauma patients.

In patients without headache, lethargy, or focal neurological deficit, a secondary complication is unlikely to develop as a result of head trauma. Imaging studies are generally not performed for asymptomatic patients.  But however, CT (computed tomography) analysis should be performed for symptomatic patients with or without focal neurological deficit.

Spinal Cord Injury

Traumatic spinal cord injury may be caused by spinal fractures, dislocated spinal fractures, hyperextension, herniation of intervertebral disc material into the channel and penetrating injuries such as firearms or stabbing.  Neurological deficits may be mild and transient, as well as severe and permanent.  Spinal fracture and spinal injury should be suspected in all cases of head trauma and multiple trauma whether come state is present or not.  By assuming at the beginning that the spinal column is unstable, it is best to keep the patient immobilized with cervical collar on a flatsurface until a careful examination and diagnostic tests are performed.

Clinical signs of the injuries of the spine or spinal cord include tenderness in the vertebrae, loss of strength in the extremities, numbness or paresthesia, respiratory disorder and hypotension. Involvement of spinal nerve roots show up in form of radiculopathy characterized by motor and sensory loss in the relevant myotome and dermatome.  Spinal cord involvement may reveal different and various clinical signs related to developing myelopathy.

A complete lesion is typically seen as a complete loss of motor and sensory functions below the level of injury and is an indication of the anatomical or physiological total loss of the spinal cord. Acute loss is characterized by areflexia, flaccidity, anesthesia and autonomic paralysis below the lesion level. Arterial hypotension developed due to the loss of sympathetic vascular tonus is a stable finding in all the losses above T5 level.

Incomplete lesions of the spine may cause loss of ipsilateral motor function and sense of position/vibration below the level of injury, as well as Brown Sequard syndrome that obviously reveals itself as pain and loss of temperature sensation in the opposite half of the body. Anatomically this condition is explained by the partial loss of the spinal cord.  Central Cord Syndrome is characterized by bilateral loss of motor function and pain and temperature sensation of the upper extremities and relatively preservation of these functions in the lower extremities.  Typically, the distal part of the upper extremities is more severely affected because the most medial parts of the corticospinal and spinothalamic systems involve the fibers of these regions.  Central cord syndrome is common following cervical hyperextension injury with or without fracture. Anterior spinal artery syndrome includes preservation of light touch sensation of position and vibration and loss of bilateral motor function and pain and temperature sensation below the lesion level. As a result of the injured anterior spinal artery, this incomplete lesion affects the bilateral anterior and lateral columns in the spinal cord region, blood supply of which is provided by this artery related to the ischemia. The most common cause of anterior spinal artery syndrome is acute cervical disc herniation.

Signs and symptoms of cauda equina compression may come up as a result of lomber spinal trauma.  Many lumbosacral radiculopathies in various severities may show up.  Motor, sensory and reflex functions may be affected in lower extremities.  Loss of strength, loss of sensation (all modalities in the regions of specific distribution of involved roots) and loss or reduction of reflexes in various severities occur.  Bladder distension caused by the paralysis of detrusor muscle in severe injuries, flaccid anal sphincter and perineal sensory loss are common in cases with severe damages.

Ileus is common with gastric distension and it requires nasogastric drainage.  Similarly, bladder distension is seen due to flaccid muscles of the bladder and pelvic floor.  By deteriorating the disposal of urine from the bladder and venous return to the heart, it will prevent the excessive distention causing significant compression on inferior vena cava and pelvic veins, which may result in systemic hypotension.

If spinal cord injury is above T5 level, blood pressure is is usually low.  This causes the denervation of the sympathetic nervous system, which leads to an increase in venous pooling and a decrease in venous return.

Tachycardia is a common compensatory response to hypotension, but bradycardia is also inevitable when the cervical spinal cord is damaged and the sympathetic input of the heart is lost. Unless a patient is symptomatic or is at risk of paralysis due to myocardial infarction or age-related or other disease that cause weakness, this type of bradycardia is not necessary to be treated.

Once the patient achieves hemodynamic balance, spinal x-rays are necessary, but the patient should remain immobile with rigid cervical collar on spine board.  Standard x-rays are performed ensuring that the cervicothoracic junction is visualized well.  A good, clear x-ray showing the whole of the spine of severely injured patients in coma and/or with multiple traumas.  Fracture regions can be examined by CT in more detail using both axial and sagittal images together.  If CT or normal x-ray reveals no abnormality and if the neurological deficit is present on the spinal cord in form of levelling, myelography or MRI should be used to identify other causes such as traumatic intervertebral disc herniation or spinal epidural hematoma after CT.

The goals of the treatment are to correct the vertebral alignment, to protect the undamaged nervous tissue, to repair the damaged nervous tissue and to provide a permanent stabilization in the vertebrae.  The correction and fixation of any fracture or slide should be the priority among these goals.

The abnormal alignment in the cervical region can always be almost corrected by skeletal traction in the neutral position.  Frequent x-rays are performed to ensure the correct alignment.

Firstly the treatment is initiated with stabilization in patients with thoracic and lumbar spinal fractures.  Stabilization is not too tight compared to cervical fractures, but in principle it is same. While avoiding bending, stretching, leaning and rotational movements, the patient is kept in straight position on the bed without moving. Typically, they have fewer systemic complications associated with neurological damage, but it is still necessary to be awake to ensure neurological improvement.

Indications for early surgery in patients with spinal cord injuries include fracture/dislocation cases that cannot be adequately corrected by closed methods, neurological worsening in a patient with incomplete lesion, a severe spinal compression caused by intramedullary mass lesion visualized by myelography or MRI and a penetrated injury with or without CSF leak.  In cases of open injury, such as stabbing and firearm injuries, the wound should be cleaned and closed, whether a complete cord injury is present or not.  Early surgery to stabilize the spine is a justified reason.  Because this provides early movement and rehabilitation.  Depending on the nature of the spinal cord injury and the level of the instability, either anterior or posterior approach may be adopted.

If closed reduction is successful and the fracture is stable, at least 3 months of external immobilization is required to ensure adequate recovery.

External immobilization is again indicated in cases in which surgical reduction and/or stabilization is mandatory.  After anterior and posterior metallic plate implantations, a rigid cervical collar can be enough. In the thoracal and lumbar region, again at least 3 months of mobilization with a plastic body jacket or plastic fixation is usually required.  Straight x-rays are used to follow up the spinal alignment and the level of fusion throughout the recovery period.

If any function of the spinal cord is protected immediately after the accident, some functions usually heal if the cord and spinal cord are not affected by the secondary injury.  In cases with complete cord lesions, the functions below the lesion level rarely return.  For these cases, rehabilitation is carried out in accordance with their own care and vocational adjustment. Long-term problems related to skin care and repetitive urinary tract infections are the causes of early death.