Chapter 11. Traumatic Brain Injury: Effects of Closed Head Injury
According to Rosenthal et. al. 1990, (in Brookshire, 1997), about 7 million people in the United States suffer traumatic brain injury (TBI) each year. Friedman, 1988, (in Love and Webb, 1992), says that there are approximately 400,000 new head injuries each year. The National Head Injury Foundation estimates that more than 500,000 people suffer TBI each year in the U.S. I cannot explain the discrepancies between them, although I am inclined to agree with the latter. Perhaps the larger figure counts all head trauma regardless of the affects of injury. When limited to serious injury then, between 400,000 and 500,000 seems logical. According to Annegers et al.,1980, (in Brookshire, 1997), the probability of subsequent TBI for people with previous brain injuries is quite high; a person with two TBI's is eight times more likely to have another than is a person who has never had head trauma. According to Davis, 2007, death from traumatic brain injury is the most common cause of death in people under thirty eight in the United states
Closed Head Injury (CHI); Effects, Symptoms, and Diagnosis
Most patients display some linguistic problems during the first few months following a closed head injury (CHI) and may exhibit deficits that can be identified using an aphasia battery. Later, however, the majority will not demonstrate confused language which seems to be the result of cognitive problems associated with right hemisphere lesions. You should expect a good deal of diversity among closed head injury patients. There is much overlap between closed head injury manifestations and those of right hemisphere lesions. A type of brain damage that occurs with closed head injury is associated with acceleration/deceleration forces (Ylvisaker and Szekeres, in Chapey, 1994). Other injuries typical of CHI are: rotational trauma, diffuse brain damage, and molecular commotion. Sometimes traumatic brain injury can effect the hippocampus in the limbic system. This can cause memory problems particularly antegrade amnesia.
Closed head injury can cause several different types of brain injury, including coup contre-coup, acceleration-deceleration trauma, rotational trauma and molecular commotion. According to Love and Webb (1992) the most predominant injury type is acceleration-deceleration trauma. Acceleration-deceleration trauma causes discrete lesions which affect only certain areas of the brain. Both rotational trauma and molecular commotion cause diffuse damage that impairs many aspects of brain functioning.
Acceleration-deceleration trauma is the most common result of CHI. It occurs when the head is accelerated and then stopped suddenly, as in a car accident, and causes discrete, focal lesions to two areas of the brain. The brain will suffer contusions at the point of direct impact and at the site directly opposite the point of impact due to the oscillation of the brain within the skull.
These injuries are similar to coup (site of contact) and contre-coup (opposite site of contact) damage, respectively. They differ in that acceleration-deceleration trauma results from the oscillation (bouncing) of the brain against bony projections on the inside of the skull. It should be noted that brain injuries may occur as a result of acceleration-deceleration trauma unaccompanied by impact. For example, babies who are shaken may suffer acceleration-deceleration brain trauma (Generalli et al., 1982, in Chapey, 1994; Ylvisaker and Shirley, in Chapey, 1994).
The prefrontal areas and the anterior portion of the temporal lobes are the parts of the brain most often affected by acceleration-deceleration trauma. Thus, if the brain is repeatedly propelled against the front part of the skull, there is likely to be major injuries.
Rotational trauma occurs when impact causes the brain to move within the cranium at a different velocity than the skull. This results in a shearing of axons by the bones of the skull. Because this type of injury damages neural connections rather than gray matter, it can affect a wide array of cerebral functions and should therefore be considered a type of diffuse injury.
Molecular commotion according to Love and Webb (1992) is a disruption in the molecular structure of the brain which may cause permanent changes in both white and gray matter. This type of diffuse brain injury may occur in the absence of discrete lesions.
Neurophysiological Consequences
The Meninges
According to Stedman (1997) epidural hemorrhaging, also called extra dural, is an accumulation of blood between the skull and the dura mater. It is usually the result of acceleration-deceleration trauma. This type of bleeding is usually arterial, commonly the middle meningeal artery a branch of the middle cerebral . This means that blood flow is very rapid and may cause a sudden increase in intra cranial pressure that results in loss of consciousness. The patient is usually unconscious immediately, then lucid briefly, then loses consciousness again from a large hematoma in the epidural space. The clot may compress cranial nerves resulting in pupillary dilation, as well as ipsalateral weakness or paralysis (Pires,1984, in Urosovich, 1984). Hemotomas from epidural bleeding are usually surgicaly aspirated often resulting in saved lives.
According to Stedman (1997), subdural hemorrhaging, or the extravasation of blood in the potential space between the dura mater and the arachnoid membrane, causes hematomas to form. Chronic hematomas may become encapsulated by neomembranes. This is often over the frontal and temporal lobes. As this type of bleeding results from damage to veins, which have lower blood pressure than arteries, subdural bleeding is much slower than epidural bleeding. According to Pires (1984), sometimes days or weeks pass before any symptoms of hemorrhaging appear. According to Bhatnagar and Andy (1995), subdural hematoma is usually due to traumatic brain injury, with bleeding from ruptured blood vessels in the arachnoid tissue below the dura mater. If not removed the blood will compress neural tissue causing infarction.
According to Love and Webb (1992), bleeding into the subarachnoid space is often the result of aneurysm. According to FitzGerald (1996), berry aneurysms bleed directly into the subarachnoid space because they originate in the circle of Willis. Strokes in those under 40 are often the result of ruptured aneurysm (FitzGerald, 1997). Traumatic brain injury is less likely to cause subarachnoid bleeding except with penetrating brain injury.
Bleeding within the structures of the brain is often the consequence of penetrating head wounds rather than closed head injury. It can also occur due to cerebral vascular accidents.This kind of hemorrhaging can occur in the cortex as well as in subcortical areas. When it is the result of closed head injury, rather than CVA it most commonly affects the frontal and temporal lobes. Most penetrating brain injuries result from high velocity missiles such as bullets. Low velocity focal injuries (blows to the head-head hitting windshield) can result in bone fragments penetrating the brain. There is a high rate of mortality following penetrating brain injury especially to the brain stem (Brookshire, 1997). They would be invariably fatal if in the medulla because of cranial nerve X which innervates circulation (heart) and respiration.
Due to the edema that follows CHI, brain matter can be forced through the tentorial notch. The notch is a cavity formed by the the tentorium cerebelli and the sphenoid bone. The tentorium is a sheath of hard tissue, formed by the dura mater. According to FitzGerald (1997), it forms a tent above the posterior fossa. It separates the cerebrum and brain stem from the cerebellum. Tentorial herniation may cause decortication or removal of cortical tissue from the underlying white matter. It may also put excessive pressure on the brain stem and thus affect cranial nerves involved in vital functions including respiration and circulation. Symptoms indicating that the brain stem is under too much pressure include severe headache, hypotension, sleepiness, loss of consciousness, bradycardia (slow heart rate), confusion, respiratory difficulties, and pupil dilation (due to pressure on the nuclei of CN III) (Bach-y-Rita 1989, Mosby, 2006).
After CHI, barbiturate induced coma may be used to manage intracranial pressure.
Release of Neurochemicals
Large amounts of neurochemicals may be released in response to CHI, just as occurs after infarction due to stroke. After CHI, the presence of excessive quantities of prostaglandin and free radicals in the brain may cause further damage (Clifton, 1989 in Bach-y-Rita, 1989).
Diachisis can occur after CHI as well as stroke.
Neurolinguistic/Neurobehavioral Symptoms
Different types of symptoms are associated with focal versus diffuse lesions caused by CHI. Of course, it is possible for a patient to suffer both focal and diffuse lesions as a result of head injury and thus display the symptoms associated with both types of damage.
If focal lesions affect the language and swallowing centers of the brain, they can cause symptoms similar to those seen as a result of a left cerebral vascular accident including apraxia, dysarthria, aphasia, dysphagia, agnosia, anomia, and dysphonia.
Focal lesions can also cause more general impairments that affect language, similar to those resulting from right hemisphere damage. These include attentional, perceptual and pragmatic deficits.
Diffuse brain injury can impair attention and perception causing problems like neglect and prosopagnosia. An inability to analyze and synthesize information and a reduction in the rate of information processing may also result from wide-spread brain damage. In addition, long term memory and problem solving may be impaired. Reasoning, both inductive and deductive, may be involved. Convergent and divergent thinking are the two main parameters of reasoning. Convergent thinking often produces single conclusions while divergent thinking is open ended e.g. how many things can you do with a toothbrush? Pragmatic problems like impaired social judgment, reduced inhibition, and poor comprehension of abstraction may occur as well. Secondary damage in CHI includes widespread or localized edema as well as slowly developing hemorrhages (Ylvisaker and Szekeres, 1994, in Chapey, 1994).
Most TBI patients have problems with long term memory. Tulving (1983) divides retrospective memory into declarative memory and procedural memory. Declarative memory is described in terms of what we know about things. For example when I tell you about Ireland I'm using declarative memory. It can be subdivided into episodic memory and semantic memory (Tulving, 1972, in Brookshire, 1997). Episodic memory is memory of single events. When they are repeated over time they go into semantic memory. An example is a parent who says "bath" every time she bathes her child. After a number of such episodes the child associates the word "bath" with the activity. At that point "bath" becomes part of semantic memory. Remembering one particular episode such as having dinner with a friend is also considered part of episodic memory.We store knowledge about the world in semantic memory. Knowing that Dublin is Ireland's capital or that Mary Robinson was the President of Ireland is stored in semantic memory. According to Brookshire (1997), impaired retrospective memory in TBI adults can be pretraumatic memory loss and/or post traumatic memory loss. The former has been called retrograde amnesia, the latter anterograde amnesia. In post traumatic memory loss the problem is getting information into long term memory. I have had a number of patients who could not remember the previous therapy session that they had that morning or that they had a visit from a family member. With pretraumatic memory loss they may not even be able to remember the family member but they will remember the previous therapy session. As you can see post traumatic memory loss is far more serious in terms of functional recovery. Procedural memory is fairly automatic. You must remember overlearned routines such as in my case, flying an airplane.
According to Clifton (1989), CHI is classified as severe, moderate, or mild based on the degree to which consciousness is impaired immediately after injury. According to Clifton (1989), severe head injury has been defined as coma for longer than six hours. Concussion defines mild head injury. The Glasgow Coma Scale, which was developed by Jennett and Teasdale (1989), is the instrument most frequently used to quantify levels of consciousness. It consists of three categories: eye opening, verbal responses and motor responses.
Glasgow Coma Scale.
A patient can receive the following scores on the eye opening scale:
4 (spontaneous)
3 (in response to voice)
2 (in response to pain)
1 (no eye opening observed)The following scores are possible on the verbal response scale:
5 (oriented)
4 (confused)
3 (inappropriate words)
2 (incomprehensible words)
1 (no verbal responses observed)These are the scores possible on the motor response scale:
6 (follows commands)
5 (localizes pain)
4 (withdraws from pain)
3 (flexion)
2 (extension)
1 (no motor responses observed)CHI is considered severe if the patient's GCS is 8 or less, indicating coma. A moderate CHI is defined as a GCS score of 9 to 12, indicating impaired consciousness without coma. A GCS of 13 to 15 Corresponds to the confusion and disorientation displayed in cases of mild CHI. Note that the Glasgow Coma Scale has prognostic value. The scores obtained on this instrument both immediately after head injury and twenty-four hours later correlate with degree of long-term impairment.
Cognitive Screening and Assessnment
The December 18th. 2012 ASHA Leader had a very good article on screening tools for cognition by Janet Schreck, CCC-SLP, a doctoral candidate at Loyola University. The Mini-Mental Status Examination was first on the list of her screening tools.
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by Janet Simon Schreck, a doctoral candidate at Loyola University