Karen Levin, Ph.D Speech Therapist, Johannesburg
This is an animal friendly practice. People who are allergic to animals OR who do not like to be around animals are unfortunately not able to attend this practice! Apologies to those who are excluded.
083 264 1697
25 Zonda Avenue,
Karen Levin, PhD
Speech-Language Therapist and Audiologist
Johannesburg, South Africa
This is an animal-friendly practice. I cannot acccomodate those who do not want to be in the presence of animals or who are allergic. Apologies to those who are excluded.
TRAUMATIC BRAIN INJURY
This page describes TBI in general. For more specific information on communication after a TBI, please click here to go to the page "Traumatic brain injury and communication impairments
Traumatic brain injury is defined as injury to the brain as a result of a closed head injury or an open brain injury. We usually restrict the use of the term TBI to include only those injuries to the brain that occur from an external force acting on the head, and do not include injuries from causes such as strokes, tumours, degenerative diseases, infections and demyelenating diseases.
The brain damage results in a variety of difficulties which are usually long term. People who have sustained a TBI can have motor, sensory, cognitive, communication, and/or psychiatric problems of various severity levels depending on the severity of the brain damage and the levels of damage to the brain.
The key word is 'traumatic" which tells us that the brain injury was caused by an event that was sudden and caused traumatic damage.
TBI is very common - it can happen to anyone at any age, but certain populations are more at risk than others. Most injuries occur in very young children, in young male adults under the age of 30, and in older persons from things like falls. Some populations of people are more at risk than others for TBI such as people with learning disabilities, people who use recreational drugs, and people who have a history of previous head injures.
In peacetime, most head injuries are CLOSED HEAD INJURIES in which the coverings of the brain (the meninges) are not damaged although the skull may be damaged. Causes include car accidents and falls.
OPEN HEAD INJURIES are usually caused by a tearing in the covering of the brain either due to pieces of the skull tearing through it, or by an external item penetrating the skull such as a bullet.
The damage caused by closed head injuries is more diffuse and widespread than the damage in open head injures which is more focal, but the damage from open head injuries can be diffuse.
There are very noticeable differences between the recovery and symptoms of open and closed head injuries.
What are primary and secondary lesions?
TBIs result in two types of damage to the brain: primary brain damage, which is damage that occurs at the time of impact (e.g., skull fracture, bleeding, blood clots), and secondary brain damage, which is damage that evolves over time after the trauma (e.g., increased blood pressure within the skull, seizures, brain swelling).
Some information on the primary lesions.
Primary lesions are the problems that are caused immediately, at the time of impact.
Diffuse axonal injury (DAI): Diffuse axonal injury is the shearing (tearing) of the brain's long connecting nerve fibers (axons) that happens when the brain shifts and rotates inside the bony skull. The damage is microscopic.
Contusions: This is bleeding on the brain. Large contusions sometimes have to be surgically removed. A coup contusion occurs near the point of impact - the skull presses on the brain which causes bleeding at that point. A contre-coup contusion occurs at a site opposite the focal point because the brain is pushed against the skull on the opposite side. The symptoms depend on the size and the site of the contusion
Lacerations: If there is a tear in the brain, we call it a laceration. These usually occur in severe head injuries
Skull fractures: There is no relationship between the severity of the skull fracture and the severity of the brain damage.
Some information on the secondary lesions:
Secondary lesions are the complications that arise from the primary lesions. We used to think that brain swelling was the reason for most of the brain damage, but that is definitely not the case today. We know a lot, but we absolutely don't have a full understanding of how the brain works, and how secondary lesions affect the person.
Cerebral oedema: This is swelling. Excess water collects in the brain tissue after trauma. Swelling occurs around the site of the trauma, on one side of the brain, or on both sides of the brain. The axonal fibres are stretched, the brain tissue is compressed, blood cells are compressed, and the brain can herniate (i.e. shifts in parts of the brain to other parts).
Raised intracranial pressure: The internal pressure of the brain can increase due to the oedema, as well as collections of blood or cerebrospinal fluid. Raised intracranial pressure leads to other complications such as herniation, and blood flow problems leading to ischemia.
Ischemia: is a restriction in blood supply to the brain tissue which causes a shortage of oxygen and food to the brain which leads to more damage).There is an extremely high (97%) incidence of ischemia following TBI. Different areas of the brain are more affected than others. The brain does not get enough glucose and oxygen for metabolism which leads to the death of brain cells.
Cerebral atrophy: Areas of the brain die off and waste away (shrink). It often happens in the frontal and temporal lobes, but also in diffuse patterns throughout the brain.
Ventricle enlargement: The ventricles are cavities within the brain filled with cerebro-spinal fluid (CSF) which acts as a cushion for the brain. CSF also supplies nutrients to the brain. CSF is produced in the brain. The brain has four ventricles: two lateral ventricles, the third ventricle and the fourth ventricle. CSF flows from the lateral ventricles into the third ventricle, then through a tube (the cerebral aqueduct) into the fourth ventricle and then the CSF flows around the spinal cord and over the surface of the brain before being re-absorbed. Following brain atrophy, the ventricles enlarge.
Bleeds: Bleeds within the brain are called 'intracranial hemorrhages' and are very common but we really only get to know that they are there when they become large. They often require emergency treatment
Rhinorrhea and otorrhea: Rhinorrhea is the leakage of CSF out of the nose, and otorrhea is leakage of CSF out of the ear. Infections are a hazard of these problems.
Epilepsy: Usually epilepsy is triggered by the scar tissue that results from a brain laceration. In some children, epilepsy post TBI occurs very soon but in adults it can appear within the first 2 years after the injury.
Vertigo: Dizziness is very common after TBI, and can be associated with vomiting. It can last for days, weeks, or for many months after TBI.
Recovery from TBI
In very general terms, we look at three stages of recovery. Recovery often follows patterns (but there are always huge individual variations).
The first is the stage of unconsciousness, which occurs immediately after the trauma. A 'coma' is a state of unconsciousness in which there is no spontaneous eye opening. Almost everyone who has sustained a TBI comes out of the coma into what is known as a 'vegetative state' characterized by (a) spontaneous eye opening (b) sleep/wake cycles while still unconscious. They then move into a more oriented phase in which awareness and purposeful behavior start, often first noticed when the person starts to fixate visually or track visually. We usually look at how long the person is unconscious which tells us a lot about the extent of the brain damage. People who have lost consciousness for seconds or minutes are often sent home from hospital quite quickly; others will be hospitalized for some time. (Note that some people unfortunately remain in the vegetative state, sometimes for years).
The second stage in recovery is the 'stage of emerging consciousness and confusion'. The person comes out of the coma, but not to full consciousness. The responsiveness to the environment and persons may start slowly, and can be erratic. Their communication at this stage is unreliable. We refer to this as 'minimally conscious state'. At this stage, usually the person moves out of acute hospital care.
Over time, the person becomes more and more responsive to the environment, but is very confused. He or she can be agitated, confused, highly distracted, and cannot regulate (control) their behaviour. On the other hand, some people can be what we call 'hypokinetic' (very little movement), under-active, and withdrawn. He or she may be disoriented and not know who they are, who people are, where they are, and what time it is - time, day, year are confused. At this stage of recovery, memory is very disturbed - we call it 'dense anterograde amnesia' or dense 'post traumatic amnesia'- persons with TBI are disoriented, cannot remember anything from one moment to the next, and cannot learn any new information. The person may not be able to remember the accident, and may be unable to lay down new memories for a period of time, so he or she may not remember that you have been to visit. The duration of this stage is an important indicator of the severity of the brain damage.
As they go on to recover even more, the person may now have more control over his or her attention, can focus more, can control behaviour more, is more oriented to people, to the place and to time, and will have some day to day memory - even if not perfect. At this stage, the person probably still needs a lot of supervision and assistance and may not cope yet at home.
The next stage of recovery is what we refer to a 'post-confusional restoration of cognitive function'. During this phase, the person who has sustained the TBI slowly improves in his or her cognitive and behavioural function and can now take on previous roles such as work or family - however, at first, these situations can be very challenging.
Post traumatic amnesia
PTA is a very, very important measure. It helps us to know when the person is conscious. It seems to be a good indicator of long term outcome. It is the time when the person (i) knows where he or she is (ii) starts to and continues to remember day to day things. It is usually long after the family is aware that the person has started to become conscious.
How long does recovery from TBI take?
Most people who had a momentary or very brief loss of consciousness are diagnosed with concussion, and will pass through the stages of recovery in anything from a few seconds, to a few minutes, or possibly a few hours. Sometimes, they remain with a headache for a while, and can also have some period of mild confusion for a while. We are starting to look more and more carefully at mTBI (mild TBI) because we seem to be getting more knowledge about possible long term effects of concussion.
Patients who have sustained a moderate or severe TBI can take weeks, months or even years to recover.
Recovery is difficult to measure, and for many people, recovery does not take them back to where they were before the trauma. Learning to live with the lasting effects of the TBI is the goal.
What are recovery scales?
Doctors and other professionals involved in the care of people who are recovering from TBI have found it useful to use published scales that track the recovery of their patients. The Glasgow Coma Scale is used in the acute stages; the Rancho Los Amigos Levels of Cognitive Functioning is probably the most commonly used throughout the recovery process, and a third is the Braintree Scale which is a simpler scale that tracks recovery from a neurological perspective.
GLASGOW COMA SCALE
Doctors and nurses use this scale in the ACUTE stages. It is very useful for monitoring recovery but not long term! The Glasgow Coma Scale is based on a 15 point scale for estimating and categorizing the outcomes of brain injury on the basis of overall social capability or dependence on others.
The test measures the motor response, verbal response and eye opening response with these values
I. Motor Response
6 – Obeys commands fully
5 – Localizes to noxious stimuli
4 – Withdraws from noxious stimuli
3 – Abnormal flexion, i.e. decorticate posturing
2 – Extensor response, i.e. decerebrate posturing
1 – No response
II. Verbal Response
5 – Alert and Oriented
4 – Confused, yet coherent, speech
3 – Inappropriate words and jumbled phrases consisting of words
2 – Incomprehensible sounds1 – No sounds
III. Eye Opening
4 – Spontaneous eye opening
3 – Eyes open to speech
2 – Eyes open to pain
1 – No eye opening
The final score is determined by adding the values of I+II+III
This number helps medical practitioners categorize the possible levels for survival, with a lower number indicating a more severe injury and a poorer prognosis. BUT please be aware that for many reasons we are very careful about not placing too much value on the GCS for predicting severity. In fact, we have evidence today that there is little association between the GCS score and the eventual outcome. The GCS is taken after the patient has been resuscitated and must be taken in the first 6 hours after the accident. Then it is taken repeatedly in the early stages. We do not use the GCS after the [patient goes home. Basically, the GCS is a measure of the persons's consciousness.