Traumatic brain injury symptoms, diagnosis and treatment

Diagnosing traumatic brain injury neurologic symptoms

In cases of traumatic brain injury detected at an early stage, an x-ray of the skull bones is the initial diagnostic technique. For evaluating the location and severity of brain tissue damage, MRI of the brain is the most suitable method. Patients with a concussion do not need to undergo MRI diagnostic procedures.

The most precise technique for detecting subarachnoid hemorrhage and its severity, assessing meningeal response to head injury, identifying brain damage, and detecting inflammatory complications of spinal injuries is lumbar puncture (LP) when compared to other methods.

The most frequent indications and manifestations of a traumatic brain injury, such as a concussion or brain contusion, are observed during the initial stage following an injury, which could be caused by events like a blow to the head, a fall, a car accident, among others:

• damage to the scalp
• abrasions and swelling
• fracture of the skull bones
• nasal discharge
• neck muscles are tense
• loss of consciousness

The outcome of a neurological evaluation could result in a diagnosis being made. In cases where the diagnosis is not yet definitive and requires further investigation, the patient may be provided with additional methods or medical tests for laboratory purposes.

Additional medical tests or laboratory investigations may be performed to further define the diagnosis of a traumatic brain injury.

• cerebrovascular Doppler ultrasonography, REG, EhoEG
• skull and cervical spines x-ray examination
• brain MRI
• brain CT
• cerebrovascular MR-angiography
• cervical spine MRI
• lumbar puncture (LP) for cerebrospinal fluid (CSF) analysis

Patients after a 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 an 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.

Intubation and severe facial swelling may preclude the ability to score eye and verbal components. For these circumstances, the score is frequently noted with a modifier, i.e. "V1t" (t = tube), or "E1c" (c = closed).

 

Glasgow Coma Scale Calculator

This calculator helps to assess a patient's level of consciousness after a head injury or other trauma.

Eye Response: Spontaneous To verbal command To pain No response

Verbal Response: Oriented Confused conversation Inappropriate words Incomprehensible sounds No response

Motor Response: Obeys commands Localizes pain Withdraws from pain Abnormal flexion (decorticate) Extensor response (decerebrate) No response

Calculate GCS

GCS Score:

 

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 abnormal and irreversible conditions such as cerebral hypoperfusion (cerebral ischemia) or hyperperfusion (brain hyperemia).
2. Changes in the volume of cerebral blood flow and systemic blood pressure lead 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 in 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 a 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 a 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 brain injury severity and adverse neurological outcome for the patient. Still little is known about the role of blood glucose 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 causes inflammation of the brain tissue in acute critical conditions involving an accumulation of neutrophils.

 

Traumatic brain injury symptoms treatment

The appropriate course of treatment for a patient diagnosed by a physician with a concussion or brain contusion will depend on the seriousness of their symptoms and the underlying causes. This may involve addressing issues such as headaches, focal neurological problems, altered consciousness levels, or other related concerns:

• bed rest
• medication treatment, including nonsteroidal anti-inflammatory drugs (NSAIDs), pain relievers, and hormones.
• trigger point injection in the neck muscles
• lumbar puncture
• physiotherapy
• occupational therapy
• reflexotherapy (acupuncture)
• surgical treatment

The procedure of lumbar puncture is employed to quickly drain cerebrospinal fluid following brain surgery or intracranial bleeding. In these situations, if there are no contraindications, a quantity of cerebrospinal fluid of 10 to 20 ml or greater can be safely collected.

Attention! If someone is experiencing persistent, severe headaches, they should seek consultation from a neurologist or neurosurgeon. It is a common mistake for family members of individuals who have suffered head injuries such as concussions, contusions, brain hemorrhages, or axonal shearing lesions to perform self-tests using tomography, Doppler, EEG, and other methods. However, this does not provide a comprehensive treatment plan, and it is recommended to consult a neurotrauma specialist, such as a neurosurgeon.