Motorcycle Accident Brain Injury

How Can the Brain be Injured from a Motorcycle Crash?

Brain Injury Florida Brain Injury is a Common and Unfortunate Result of a Florida Motorcycle Accident.Brain Injury Florida Brain Injury is a Common and Unfortunate Result of a Florida Motorcycle Accident.

In the United States traumatic brain injury (TBI) is a leading cause of death for persons under age 45. TBI occurs every 15 seconds. Approximately 5 million Americans currently suffer some form of TBI disability. The leading causes of TBI are motor vehicle accidents, falls, and sports injuries. While the brain is by far the most complex object on earth, it is soft and vulnerable with a consistency of firm pudding. A concussion is a sudden trauma-induced alteration of the alert state. The person may be unable to concentrate or be confused for a few seconds, or completely lose consciousness and fall down. The brain is capable of recovering from a concussion. How much force is necessary to cause permanent brain damage is under study, and hence still unclear. Over the years, professional boxers suffer permanent brain damage. The force of a professional boxer’s fist is equivalent to being hit with a 13 pound bowling ball traveling 20 miles per hour, about 52 g’s. Plopping down into an easy chair can generate up to 10 g’s. So, it seems that somewhere between 10 and 50 g’s is the threshold to permanent brain injury. This does not mean that accelerations over 50 g’s have to cause permanent brain damage. Football players are subjected to 200 g’s, and Indy race car drivers have been subjected to 80 g’s without permanent injury, but they were wearing helmets.Whiplash seems to be particularly damaging to the brain. Woodpeckers smack their heads against trees with 1200 g’s of force without suffering brain damage. Part of the reason is that they keep their heads in the plane of their body; the head does not rotate in a “yes-no” manner during the pecking. If there were some way to stabilize the head when driving – akin to wearing a mail suit from the Middle Ages – more people would walk away from automobile accidents without serious brain injury.The brain is vulnerable to traumatic damage in two ways. The cerebral cortex can become bruised – contused – when the head strikes a hard object (or a hard objects strikes the head). Or, the deep white matter can suffer diffuse axonal injury when the head is whiplashed without hitting a hard object (or being hit by one). In serious whiplash injuries, the axons are stretched so much that they are damaged.Cerebral contusions tend to occur at the tips of the frontal and temporal lobes where they bang up against the interior of the skull. Diffuse axonal injury occurs more toward the center of the brain where axons are subjected to maximal stretching.

Common Types of Brain Injuries from a Motorcycle Accident in Florida

Direct Trauma Brain Injury – Any force that penetrates or fractures the skull may cause severe brain injury as destructive shock waves are sent through the brain matter. Displaced fractures of the skull can also push bone into the brain, causing tissue damage.

Direct trauma to the brain can occur when the skull strikes, for example, the floor in a fall accident or strikes a steering wheel in a car accident. Although the skull may not be penetrated or fractured in these types of accidents, the forces imparted to the brain can cause the brain to collide against the inside of the hard skull. When a moving head comes to a quick stop, the brain continues in its movement, striking the interior of the skull. This can cause bruising of the brain (a contusion) and bleeding (hemorrhage). Injury in these types of accidents occurs in parts of the brain closest to the point of impact, quite often the tips of the frontal and temporal lobes. In cases of blunt head trauma the brain can also be injured directly opposite the site of trauma — on the other side of the brain, an injury known as contrecoup. This injury typically occurs when a moving head strikes a stationary object like the windshield. At impact the brain opposite the site of impact is pulled away from the skull, injuring the brain there.Indirect Trauma – Medical research has discovered another mechanism of brain injury besides direct blunt trauma to the skull. The well-known phenomenon of the Shaken Baby Syndrome is an example. Severe shaking greatly stretches and damages delicate nerve cells, at times causing very significant injury or even death. In adults, severe whiplash can involve severe forces that may shake or rotate the brain enough to cause permanent brain damage.Diffuse Axonal Injury – The brain consists of billions of nerve cells located in the gray matter which communicate with distant nerve cells through long nerve fibers called axons, composing the white matter. Severe sudden twisting or torquing of the brain, as occurs in a sudden acceleration/deceleration – whiplash — accident, can stretch, twist, and damage these delicate axonal fibers. Under the microscope the axonal damage is called Diffuse Axonal Injury (DAI). Although diffuse axonal injury generally results from a severe whiplash injury that renders a patient comatose, recent studies have shown that diffuse axonal injury can also occur – but to a lesser degree — when there has been only brief loss of consciousness (LOC). Because Diffuse Axonal Injury causes microscopic damage, it cannot be visualized on CT or MRI scans.A second method of how the brain can be injured in high speed velocity change scenarios (a fall from a great height, high speed car accident) is called “Isotropic Stress.” Whereas diffuse axonal injury involves the deforming or stretching of the brain tissue, resulting in tearing, isotropic stress causes damage through a “pulse” or “pressure wave” that moves through the brain at extraordinarily high speeds. The damage is caused by a sudden change in the density of the inside of an individual brain cell. The instant compression causes damage to the internal structures of the brain cells.Many of these same types of injuries have been discovered and treated in veterans returning from the Iraq war. They have often been exposed to the proximity blast of explosive charges. The pressure or pulse from the explosion moves through their body and as it move through the brain it causes damage to the cells. Although many of these soldiers look “fine” and have no bleeding, they can and will suffer serious brain injury as a result.Because of the large number of veterans injured in this way, lots of research is being done on this type of brain injury at the present time and there should be studies available for an update on this new insight into TBI in mid-2008.Hypoxia or Toxic Substance Exposure – The brain is more susceptible to injury through lack of oxygen (hypoxia) than any other part of the body. Hypoxia can occur in conjunction with other injuries (heart attack) or from any other situation where breathing or oxygen intake is impaired. Damage from hypoxia is often seen in the hippocampus, an area of the brain necessary for laying down new memories. Exposure to toxic chemicals (lead, toluene, carbon monoxide, among many others) can also cause brain damage, depending on the level of exposure and the duration of exposure, the combination of which is called the “dose.”Secondary Types of Brain InjuryIn addition to direct neural damage discussed above, injury to the brain can also result as a secondary phenomenon following injury to non-neurologic structures.

Edema Brain Injury – is a swelling of the brain. Swelling of the brain becomes dangerous when the swelling causes a rise in intracranial pressure which prevents blood from entering the skull to deliver glucose and oxygen to the brain. Sustained high intracranial pressure can be relieved through medication, or in more severe cases, by placing a hole in the skull to drain off some of the high-pressure cerebrospinal fluid.

Hematoma – is a collection of blood due to tissue injury or the tearing of a blood vessel. CT scans done at the hospital are particularly effective in detecting brain bleeds. Bleeding into the brain after trauma can occur days after the patient is released from the emergency room. The dura is a tough membrane that covers the entire brain and spinal cord. A blood clot that develops outside the dura, between the skull and dura, is known as an epidural hematoma. A blood clot that develops between the dura and the brain is called a subdural hematoma. Gently resting against the brain itself is a thin, delicate membrane called the arachnoid. Underneath the arachnoid, between the arachnoid and the brain its self, is cerebrospinal fluid bathing and circulating around the brain. Blood leaking into the cerebrospinal fluid is known as a sub-arachnoid hemorrhage.

Hydrocephalus and Hygroma – are collections of fluid in and around the brain. The brain is hollow; the interior cavities, called ventricles, contain cerebrospinal fluid circulating from the ventricles up over the surface of the brain where the cerebrospinal fluid is absorbed. If blood somehow gets into the cerebrospinal fluid and blocks the spinal fluid absorption sites, spinal fluid will back up into the ventricles, enlarging them – a condition called hydrocephalus. If the pressure inside the ventricles becomes excessive (risking damage to the brain), a tube may need to be inserted into the ventricles to relieve the pressure. A hygroma is a localized fluid buildup usually in the subdural space. Again, if pressure in the hygroma presses against the brain, surgery may be necessary to relieve the pressure.

How do I know if a Brain Injury Occurred?

Unfortunately, there are no medically accepted criteria that can predict permanent brain damage from a particular trauma. The factors doctors take into consideration, however, include the following. Keep in mind that normal findings on the tests below do not necessarily mean that no brain injury occurred.

Loss of Consciousness (LOC) – loss of consciousness means loss of conscious awareness. Hence, loss of consciousness can range from being briefly dazed to several days of coma. Focal head trauma – a bullet – can permanently damage an entire cerebral hemisphere without loss of consciousness, but in blunt head trauma loss of consciousness is usually, but not always, necessary to permanently damage the brain. Generally speaking, the longer a period of unconsciousness, the more severe the injury. Medical providers at the scene of an accident tally up a “Glasgow Coma Scale” of the patients neurologic status, which can range from a low of 3 (deeply comatose) to a normal value of 15. The Glasgow Coma Scale is helpful in predicting a patient’s ultimate outcome — the lower the score the worse the outlook.

Post Traumatic Amnesia (PTA) – loss of memory for events prior to the injury (retrograde amnesia) and events following the injury (anterograde amnesia) frequently occur after head injury. In general, a patient with longer periods of post traumatic amnesia tends to have more of a severe injury. Studies have shown that individuals are not good at estimating their own length of amnesia (Gronwall 1980). Therefore, family members should make note of any anterograde or retrograde amnesia and track its improvement.

Concussion – a concussion is an alteration of conscious awareness after head trauma. The collection of symptoms following a concussion is called the postconcussion syndrome (PCS), and include dizziness, nausea, vomiting, headache, disorientation, forgetfulness, irritability, depression, mood swings, insomnia, and loss of libido. Most cases of PCS resolve after a few months, but approximately 20% of cases can involve longer term problems.

Encephalopathy – a disturbance of brain function indicating something is wrong with both sides of the brain’s gray matter. Signs of encephalopathy include stupor, confusion, memory loss, inattention, agitation, and inappropriate aggression. An encephalopathy after head trauma only means the brain is not functioning properly. It does not necessarily mean the dysfunction is permanent.

Focal Neurologic Signs – signs that allow a doctor to conclude that a specific part of the brain is not functioning.

Seizure – nerve cells communicate with one another electrically and chemically. One nerve sends an electrical discharge along its axon to stimulate another distant nerve. The actually stimulation is done chemically. When the electrical discharge reaches the end of the axon, the electricity causes the axonal tip to spit a chemical “neurotransmitter” at receptor sites on the next nerve cell. All this takes place in a nice orderly fashion. A “grand mal” seizure occurs when every nerve cell in the brain rapidly fires electrical discharges at one another. The resulting chaos causes the patient to lose consciousness, fall down, and convulse. The same uncontrolled discharges in a focal area of the brain may cause the patient to experience or do what function that focal area normally controls. Such “focal” or “partial” seizures may manifest as recurrent bouts of numbness, fear, anxiety, a forced memory, jerking of a limb or face, lip smacking, sudden staring spells, or inability to speak.

PERL – medical personnel commonly test an individual with a head injury to see if the Pupils are Equal and Reactive to Light (PERL). Unequal pupils or unreactive pupils in a comatose patient after a head injury can signify a dangerous rise in intracranial pressure due to swelling, hematoma, hydrocephalus, etc. Urgent lifesaving surgery is often necessary to relieve the elevated pressure.

There has been a hypothesis that a person struck in the head who suffers facial fractures may have decreased injury to the brain because of the fracture being a “shock absorber” to the brain. However, a recent study showed that the outcome of those with facial fractures verses non-fractures was the same. The presence of fractures of the face does not favor a better outcome.

A study from 2002 confirmed what was previously believed in regard to the outcome of the elderly with traumatic brain injury. The mortality rate from TBI is higher in the geriatric population at all levels of head injury. There outcome at the time of hospital discharge is worse. This outcome is independent of any other co-factor such as age or other disease.

Brain Injury Symptom Checklist

A wide variety of symptoms can occur after “brain injury.” The nature of the symptoms depends, in large part, on where the brain has been injured. Below find a list of possible physical and cognitive symptoms which can arise from damage to specific areas of the brain: Frontal Lobe: Forehead

  • Loss of simple movement of various body parts (Paralysis).
  • Inability to plan a sequence of complex movements needed to complete multi-stepped tasks, such as making coffee (Sequencing).
  • Loss of spontaneity in interacting with others.
  • Loss of flexibility in thinking.
  • Persistence of a single thought (Perseveration).
  • Inability to focus on task (Attending).
  • Mood changes (Emotionally Labile).
  • Changes in social behavior.
  • Changes in personality.
  • Difficulty with problem solving.
  • Inability to express language (Broca’s Aphasia).

Parietal Lobe: near the back and top of the head

  • Inability to attend to more than one object at a time.
  • Inability to name an object (Anomia).
  • Inability to locate the words for writing (Agraphia).
  • Problems with reading (Alexia).
  • Difficulty with drawing objects.
  • Difficulty in distinguishing left from right.
  • Difficulty with doing mathematics (Dyscalculia).
  • Lack of awareness of certain body parts and/or surrounding space (Apraxia) that leads to difficulties in self-care.
  • Inability to focus visual attention.
  • Difficulties with eye and hand coordination.

Occipital Lobes: most posterior, at the back of the head

  • Defects in vision (Visual Field Cuts).
  • Difficulty with locating objects in environment.
  • Difficulty with identifying colors (Color Agnosia).
  • Production of hallucinations.
  • Visual illusions – inaccurately seeing objects.
  • Word blindness – inability to recognize words.
  • Difficulty in recognizing drawn objects.
  • Inability to recognize the movement of object (Movement Agnosia).
  • Difficulties with reading and writing.

Temporal Lobes: side of head above ears

  • Difficulty in recognizing faces (Prosopagnosia).
  • Difficulty in understanding spoken words (Wernicke’s Aphasia).
  • Disturbance with selective attention to what we see and hear.
  • Difficulty with identification of, and verbalization about objects.
  • Short term memory loss.
  • Interference with long term memory.
  • Increased and decreased interest in sexual behavior.
  • Inability to categorize objects (Categorization).
  • Right lobe damage can cause persistent talking.
  • Increased aggressive behavior.

Brain Stem: deep within the brain

  • Decreased vital capacity in breathing, important for speech.
  • Swallowing food and water (Dysphagia).
  • Difficulty with organization/perception of the environment.
  • Problems with balance and movement.
  • Dizziness and nausea (Vertigo).
  • Sleeping difficulties (Insomnia, sleep apnea).

Cerebellum: base of the skull

  • Loss of ability to coordinate fine movements.
  • Loss of ability to walk.
  • Inability to reach out and grab objects.
  • Tremors.
  • Dizziness (Vertigo).
  • Slurred Speech (Scanning Speech).
  • Inability to make rapid movements.
COMA: SOME FACTS

The outcome of a patient can be associated with their best response in the first twenty-four hours after injury. Using the Glasgow Coma Scale (3 to 15, with 3 being a person in a coma with the lowest possible score, and 15 being a normal appearing person) research shows that if the best scale is 3 to 4 after twenty four hours, 87% of those individuals will either die or remain in a vegetative state and only 7% will had a moderate disability or good recovery. In patients with a scale from 5 to 7, 53% will die or remain in a vegetative state, while 34% will have a moderate disability and/or good recovery. In patients with a Glasgow Coma Scale of 8 to 10, 27% will die or remain in a coma, while 68% will have a moderate disability and/or good recovery. In patients who have a scale from 11 to 15, only 7% will be expected to die or remain in a coma, while 87% would expect to have at least a moderate disability and/or good recovery (remembering again that this is not an exact science).

Most comas end with eye opening and regaining of consciousness, however 10% of patients who open there eyes fail to regain consciousness. (Sometimes called Apallic Syndrome). These patients do not usually respond to environmental stimuli.

There is a syndrome which occurs in children, who after waking from the coma, display delayed recovery of consciousness in response to the psychological stresses of being in the hospital, rather then continued biological cause.

Studies show that patients remaining in a vegetative state for at least one year after injury are unlikely to gain consciousness, although they may live for many years. Patients over 40 years of age have a poorer rate of recovery than younger patients, post coma.

Absence of eye opening in the first thirty days after injury is indicative of a poor prognosis.

90% of brain injured patients who are vegetative for one month or longer will fail to improve to a state better than severe disability. However, two thirds of patients who were unconsciousness for two weeks or less may make a moderate to good recovery.

SPECT Scan can be useful in examining the brain of a person in a coma, to see if there are abnormalities in cerebral blood flow.

CT or MRI Scan showing swelling, midline shift, and mass lesions may be evidence of a more prolonged coma. Likewise, enlargement of the ventricular system (the open spaces in the folds of the brain) and cerebroatrophy found months after the injury are associated with poor results.

Apallic patients (open eyes, non-responsive) can benefit from rehabilitation involving “sensory stimulation.” Studies indicate these types of programs are helpful for patients who are at the boundary of coma and wakefulness.

The common cause of coma is oxygen deprivation. Anoxia refers to a complete absence of available oxygen, while hypoxia describes someone who had available oxygen but at reduced levels for a period of time. Anoxemia describes when a person’s blood supply (rather than lungs) lacks oxygen. Oxygen deprivation lasting longer than five to ten minutes can be fatal. Almost all persons surviving five minutes or more of complete oxygen depravation or 15 minutes of “substantial” hypoxia sustain permanent brain damage (J.N. Walton, 1994). Those who do not end up in a coma typically have impaired learning ability and retrieval problems. Visual defects are not uncommon. PET studies and CT scanning can show damage in the area of the cerebellum and basal ganglia in severely impaired patients.

Therapeutic Hypothermia (artificial cooling of the body) has been thought to improve outcome of patients with severe head injury. However, recent studies have been in conflict. A 2002 study from the Netherlands (Tolderman, K.H. 2002) used this method on 136 patients with were in a coma and had high inter-cranial pressure (ICP). Their findings were that artificial cooling can significantly improve survival and neurological outcome in patients with severe head injury, when used in a protocol with great attention to the prevention of side affects from cooling.

Another thing to remember is the general rule that regardless of the cause of damages, the more rapid the onset of the condition, the more severe and wide spread its effects will be. (Ajuriagurerra, 1960; A. Smith 1984). In other words, using a stroke as an example, if the person immediately drops into unconsciousness, the outcome would, on average, be worse than someone whose stoke came over time.

Factors influencing outcome of severe head injury were accounted for in a recent study. A strong predictive factor of whether or not those with severe head injury would survive or not involve the pupils. 90% of patients who had bilaterally dilated pupils (not reacting to light) on admission died. 66% of the patients with bilaterally “constricted” pupils at the time of admission died. Only 20% of patients with severe head injury who had normal pupil reaction to light at time of admission died. Therefore, this aspect of outcome could be used to determine both mortality and outcome of coma.

There has been speculation that the presence of traumatic sub-arachnoid hemorrhage (tSh) on admission to the hospital predicted a poorer outcome than a patient without such a hemorrhage. A study (Servadei, F. 2002) supports the idea that death among patients with sub-arachnoid hemorrhage is related to the severity of the initial brain damage, rather than to the effects of delayed casospasms and secondary brain damage. The presence of such a hemorrhage on admission warrants a poorer outlook.

CT scans often fail to show brain stem lesions. Recent studies on MRI of severely brain injured coma patients show that death was closely linked to the presence of bilateral pontine lesions. Even severe destruction of the supratentorial white matter as shown on MRI was not related to increased death rates, as long as the brain stem itself is spared (Firshing, R. 2002).

Many patients with traumatic brain injury suffer defuse traumatic brain swelling (DTBS). This can lead to changes in the size of the brain ventricles (the open spaces within the brain). Doctors found a direct correlation between changes in the third ventricle and outcome. All of the things being equal, changes in that area of the brain due to swelling suggest a poorer outcome for that patient. The outcome of children fared much better than adults in this study.

Multimodal-early-onset-simulation (MEOS) in early rehabilitation on coma patients is found to be sensitive in identifying some predictions of favorable or unfavorable outcome. The data seems to support the hypothesis that the absence of any response to external stimuli is indicative of an unfavorable outcome. (The coma patients were followed two years after injury.) The comas lasted from 8 to 41 days. The average initial Glasgow Coma Scale was 6.6. Follow-up on 14 patients showed that one remained in a vegetative state, 2 exhibited severe neurological deficits and were dependant on care, 6 sustained major functional deficits but were able to return to perform the task of everyday life on their own. Two patients reached slightly higher levels then that, 2 patients returned to their former jobs).

A study from 2002 (Mosenthal, A.C. 2002) confirmed what was previously believed in regard to the outcome of the elderly with traumatic brain injury. The mortality rate from TBI is higher in the geriatric population at all levels of head injury. The outcome at the time of hospital discharge is worse. This outcome is independent of any other co-factor such as age or other disease.