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Traumatic brain injury symptoms, diagnosis and treatment

Traumatic brain injury types and causes

Research is beginning to shed more light on the cognitive and physiological effects of concussions, a type of traumatic brain injury caused by a blow to the head or other event that causes the brain to shake inside of the skull. Normally, the brain is protected by the cerebrospinal fluid (CSF) that surrounds it, as well as the skull, which acts like armor. But when the head or body experience extreme impact – such as a football tackle or car accident – the brain can crash into the skull, causing bruising, bleeding and/or swelling.

When the head's motion suddenly stops, the head jolts forward and the brain bangs against the skull, bruising the brain. The brain compresses against the skull again when it rebounds (coup-contrecoup injury). This can cause the brain tissue to swell. The tissue lacks the room to expand, causing pressure in the skull. Compression of the brain hinders the normal blood circulation in it, which further enhances its swelling.

The mechanism of brain concussion or contusion with the neck ligaments and muscles whiplash trauma during impact.

Head injury can be dangerous for human health and life, if this will be a brain injury (traumatic brain injury – TBI). Types of head injuries:

  • Concussion
  • Contusion
  • Brain hemorrhage
  • Axonal shearing lesions
  • Skull fractures
  • Cranial nerve injuries
  • Seizures
  • Subdural and epidural hematomas

All kinds of brain injuries are diagnosed by physicians and neurosurgeons require assigning an appropriate conservative or surgical treatment. In our clinic, you can take a full course of rehabilitation after traumatic brain and spinal cord injury.

All kinds of brain injuries are diagnosed by physicians and neurosurgeons require assigning an appropriate conservative or surgical treatment.

In our clinic, you can take a full course of rehabilitation after traumatic brain and spinal cord injury.

Skull CT scan revealed impressed fracture of the frontal bone in the region of the frontal sinus with damage to the left orbit roof.

Concussion occurs when a direct blow or sudden deceleration of the head. This leads to disruption of the brain function:

  • loss of consciousness
  • alteration of consciousness
  • anterograde and retrograde (posttraumatic) amnesia (loss of memory about a period of time before or after the concussion)
  • nausea with vomiting
  • headache
  • nystagmus

With such a severe brain injury as a contusion of the brain is possible fracture of the cranial vault or skull base fracture with liquorrhea (outflow of cerebrospinal fluid from ear or nose).

There are soputsvuyuschie brain injuries damage the cranial nerves from mechanical injury of the nerve or bone fragments if damaged cranial bones.

More frequently with traumatic brain injury suffer branch of the trigeminal nerve and facial nerve in mind the features of their anatomical location (exit points from the cranial cavity).

Skull fractures with brain contusion.

Diagnosing traumatic brain injury neurologic symptoms

Still at an early stage diagnosis in traumatic brain injury the first diagnostic method is x-ray of the skull bones. To study the location and extent of damage to brain tissue is best suited MRI of the brain. When a concussion conduct diagnostic procedures MRI of the brain the patient is not required.

Lumbar puncture (LP), the most accurate, compared with other methods to identify subarachnoid hemorrhage and degree of severity, to identify the reaction of the meninges on head injury, to detect brain injury and inflammatory complications of spinal injuries.

Routine x-ray examination disclose skull fractures.

The most common signs and symptoms of traumatic brain injury (concussion, contusion of the brain) occurring in the acute period after injury (blow to the head, a fall, car accident, etc.):

  • damage to the scalp
  • abrasions and swelling
  • fracture of the skull bones
  • nasal discharge
  • neck muscles are tense
  • loss of consciousness
Head injury clinical syndromes and symptoms.

According to the results of neurological examination may already be diagnosed. If the diagnosis is preliminary and will require clarification, the patient will be given additional tools or laboratory medical tests purposes.

Possible additional instrumental or laboratory medical tests purposes to clarify the diagnosis of traumatic brain injury:

Patients after head injury with persistent confusion, behavioral changes and subnormal alertness, extreme dizziness or focal neurologic signs (hemiparesis) should be admitted to the hospital and soon thereafter have a MRI or CT scan.

 

Glasgow Coma Scale (GCS)

In assessing the severity of the injury of the brain in a patient experts consider the level of neurological deficit (loss of brain functions) and the level of clarity of consciousness. For ease of evaluation in clinical practice, all these parameters (focal neurological symptoms, level of consciousness) were reduced in the table neurosurgeons (Professor Graham Teasdale and Bryan J. Jennett) from the University of Glasgow in 1974.

Glasgow Coma Scale (GCS) for head injury:

Index
Responses
Score
Motion (M)
Spontaneous movements on command 6
Expedient repulsion in response to pain 5
Limb withdrawal in response to pain 4
Abnormal flexion to pain (decortication) 3
Abnormal extension to pain (decerebration) 2
No motor response 1
Verbal (V)
Orientation in space and time 5
Awry speech, disorientation 4
Utters incomprehensible words 3
Utters incomprehensible sounds 2
No verbal response 1
Eye opening (E)
Spontaneous 4
On verbal command 3
On pain 2
Do not open your eyes 1
Total score
  3–15

Note: Coma score = M + V + E. Patients scoring 3 or 4 have an 85% chance of dying or remaining vegetative, whereas scores >11 indicate only a 5–10% likelihood of death or vegetative state and 85% chance of moderate disability or good recovery. Intermediate scores correlate with proportional chances of recovery.

 

Classification of TBI based on multiple factors. Alternate scales for TBI severity.

Severity Structural Imaging (MRI, CT) Loss of Consciousness Alteration of Consciousness Posttraumatic amnesia (PTA) Glasgow Coma Scale (GCS)
Mild Normal 0–30 min (<20 min – 1 hr) Moment <24 hours <24 hr 13–15
Moderate Normal or Abnormal >30 min but <24 hours >24 hours 1–7 days 9–12
Severe Normal or Abnormal >24 hrs >24 hours >7 days 3–8

 

Pathophysiological changes and critical care in traumatic brain injury

  1. Autoregulation of cerebral blood flow is one of the most important systems to maintain a balance of intracranial pressure. Small brain vessels respond to the hydrostatic pressure and regulate its tone to maintain a constant blood flow between the mean arterial pressures of 60 to 160 mm Hg. If in severe brain injury pressure regulation curve shifts to the right, random changes in systemic blood pressure may lead to severe and linear changes in cerebral blood flow, that lead to an abnormal and irreversible conditions such as cerebral hypoperfusion (cerebral ischemia) or hyperperfusion (brain hyperemia).
  2. Changes in volume of cerebral blood flow and systemic blood pressure leads cerebral vessels to expansion (vasodilation) or narrowing (vasoconstriction). Cerebral vasodilation (expansion of the vascular lumen) can lead to a reduction in systemic blood pressure. This causes an increase in cerebral blood volume and the rise in intracranial pressure. Such vascular reaction may also be initiated by hypoxemia, dehydration, or hypocapnia (due to hyperventilation therapy).
  3. Reduced cerebral perfusion pressure causes brains blood vessels vasodilation and the subsequent increase in cerebral blood volume. Reduced cerebral perfusion pressure is often associated with a reduction in systemic blood pressure. Exceed the capacity of autoregulation, hyperperfusion may increase the risk of brain hyperemia. Conversely, a drop in systemic blood pressure below the limit of its ability to correct the body may decrease cerebral perfusion pressure and cause cerebral ischemia.
  4. Excessive hyperventilation causes vasoconstriction and a decrease of cerebral blood flow that leads to cerebral ischemia. As a result of cerebrovascular sensitivity to blood CO2 levels, the brain blood vessels dilation, caused by an increase in the partial pressure of carbon dioxide (PaCO2), may increase intracranial pressure and help to increase blood volume in the brain (cerebral edema). If this happens, the neurological outcome for patients with severe traumatic brain injury can be poor. On the other hand, when the partial pressure of carbon dioxide (PaCO2) in the blood drops, brain vessels vasoconstriction, which leads to a decrease in brain blood volume and ultimately a drop in intracranial pressure.
  5. The increase in endogenous catecholamines (sympathetic induced catecholamines release) causes vasoconstriction of peripheral vessels, which increases systemic arterial pressure (neurogenic hypertension) after traumatic brain injury (TBI). As a result, the systemic blood pressure to be maintained, despite the presence of hypovolemia. Mannit is an osmotic diuretic, has historically been used in patients with increased intracranial pressure (ICP). When used inappropriately, however, mannitol causes excessive intravascular dehydration. As a result of dehydration and hemodynamic disturbances formed an unstable state of cerebral blood flow with sudden episodes of hypotension. To prevent catastrophic sudden drop in blood pressure (hypotension) after traumatic brain injury (TBI), should avoid the routine use of mannitol and intravascular dehydration.
  6. Hyperglycemia also often develops after severe brain damage or similar causing stress for the body events. High blood glucose levels after a traumatic brain injury (TBI), appears to be associated with a higher degree of the brain injury severity and adverse neurological outcome for the patient. Still little is known about the role of blood glucose in in the formation of secondary mechanisms of neuronal damage after brain injury. The best time to start the use of glucose-containing fluids to maintain nutrition is also questionable, since the acute hyperglycemia (elevated blood glucose level) can alter the neurological outcome for the patient. It remains to be seen whether the only one capable of hyperglycemia cause inflammation of the brain tissue in acute critical conditions involving accumulation of neutrophils.

 

Traumatic brain injury symptoms treatment

Depending on the severity of symptoms and causes symptoms of headache, focal neurological disorders in, status, level of consciousness disorders in a patient with a confirmed physician diagnosis concussion and contusion of the brain, the following therapeutic action:

Lumbar puncture is used for mesurment and management of raised intracranial pressure (ICP), rupid liquor sanation after intracranial hemorrhage.

Lumbar puncture is used for the rapid snstion of cerebrospinal fluid after intracranial hemorrhage or brain surgery. In such cases – in the absence of contraindications – recovered to 10–20 ml of cerebrospinal fluid and more.

warning Attention! If there are complaints about the long-term or chronic, as well as severe headaches should apply to a neurologist or neurosurgeon for consultation in the first place. Very common misconception action by relatives of patients with head injury (concussion, contusion, brain hemorrhage and axonal shearing lesions), when the self-test begins with the holding tomography Doppler, EEG, etc. There is no hint of an attempt of full-time treatment, consult a specialist in neurotrauma – a neurosurgeon.