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Myasthenia Gravis

Myasthenia Gravis is an autoimmune condition of the nerve junctions. The condition is present in approximately 1:100,000 people in the United States. While some doctors will summarily reject the idea that an autoimmune condition can be caused by trauma, the truth is that the scientific literature on myasthenia gravis proves that this condition can either be caused, or aggravated both by the trauma of a collision, or the treatment rendered in response to injuries for that trauma. The most recent medical text dedicated solely to Myasthenia Gravis notes that of the 23% of Myasthenia Gravis cases which have a known cause 3% are triggered by physical trauma, and another 4% by emotional trauma. But, the case for aggravation due to trauma, and medical treatment is even stronger. Our firm has handled a clear case of traumatic aggravation of myasthenia gravis after an auto accident. In that case, our client was never diagnosed with Myasthenia Gravis prior to the collision, but had eye droop symptoms (typically the first sign of MG) 10 years prior to the collision, but with negative lab tests only two years prior to the collision. After a very serious collision, our client was subjected to a series of treatments known as aggravating factors for Myasthenia Gravis, including Surgery, General Anesthetic, Morphine, antibiotics, muscle relaxants, and several others. In all, the client had 13 of the 16 known aggravating factors as a direct result of the collision, triggering a severe aggravation of the condition. This aggravation required lifetime home care for a woman who was previously completely independent. Dr. DeShaw is presently working on publishing this case study in a medical journal, since only one other case has ever been reported at Johns Hopkins Medical School.

If you have a Myasthenia Gravis case, and would like to retain our firm to assist in the matter, either as the sole firm, or as co-counsel, please contact us at (503) 227-1233.

Post Concussion Syndrome

Post Concussion Syndrome, is a sequela of a mild traumatic brain injury (MTBI) or Closed Head Injury. As you will note in Illustration 1 below, the brain suffers injury in instances when the head moves rapidly enough to allow the brain to move through its protective fluid barrier striking the inside bones of the cranium, even when the head itself does not strike an exterior object.

The Merck Manual, states the following about post-concussion syndrome:

After a mild head injury, headache, dizziness, difficulty in concentration, variable amnesia, depression, apathy, and anxiety are common, more so than after severe head injuries. Considerable disability can result. The part played by organic brain damage is unclear. Recent careful studies suggest that even mild trauma can cause neuronal damage. Epidemiologic studies suggest that the incidence of post-concussion syndrome is unrelated to the potential for compensation for injury. The benefits of drug or psychiatric treatment are uncertain. Symptoms commonly persist after compensation claims are settled.

In Whiplash Injuries: Cervical Acceleration / Deceleration Syndrome, Dr. Arthur Croft one of the foremost experts on automobile injuries in the world, lists additional symptoms as follows:

Headaches, dizziness, memory loss, inability to concentrate, sleep disorders, irritability, lightheadedness, vertigo or dizziness, neck pain, photophobia, phonophobia, tinnitus, easy distractibility, impaired comprehension, forgetfulness, impaired logical thought, difficulty with new or abstract concepts, easy fatiguability, apathy, outburst of anger, mood swings, depression, loss of libido, personality change and intolerance to alcohol.

This condition, while considered rare by many doctors, is not rare at all for those who know what to look for. Since we deal with a large number of brain injuries, we know what to consider. Based on the available medical research in this area, Dr. DeShaw has compiled a standard set of questions we ask every new client. Due to this level of investigation into each client's injuries, and because we deal with more serious injury cases, approximately 60% of all our clients meet the diagnostic criteria for some variety of traumatic brain injury like Post Concussion Syndrome, an often debilitating brain injury. A large percentage of these cases are missed by the treating physician.

According to the scientific research, most post concussion symptoms resolve within seven months, and there is a period out to 24 months where it is considered possible to still make some mild improvements. After 24 months, residual symptoms are generally considered permanent damage. But, the expected period of improvement, and the likelihood of a person's ability to improve subsequent to PCS or any other type of Traumatic Brain Injury is largely dependent upon the region of the brain injured in the accident. Generally frontal lobe damage heals more quickly and has a better chance of healing more completely than Temporal lobe damage for instance. This provides one of many reasons why injuries in side impact accidents, or accidents which occur when the head is turned, result in greater than expected injuries.

PCS is a frustrating condition for many modern doctors because it requires time and work to diagnose it. Moreover, there is no new technology which can properly diagnose it. Some researchers have been working on imaging to confirm the presence of mild traumatic brain injuries like PCS with only minor success within one month of the injury for PET and SPECT scans. These imaging methods have been successful as glucose uptake in the brain drops to coma levels in PCS patients. Conventional CT and MRI do not detect the injury because PCS is a cellular level injury and these devices are too crude currently to be able to detect the minute bleeding and damage which occurs in PCS. So, it is not unusual to have a completely normal CT or MRI study of your brain, and still have a mild traumatic brain injury.

Where is the head injury located? Only a doctor, or neuropsychologist can tell. But, consider the following:

Frontal Lobe:

• 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:

• 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:

• 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:

• 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 catagorize objects (Categorization).
• Right lobe damage can cause persistent talking.
• Increased aggressive behavior.

Brain Stem:

• 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:

• 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.

If you have a traumatic brain injury case, you will need a lawyer who fully understands these conditions. Please feel free to call us today at (503) 227-1233 to set up your free consultation, or fill out our online case evaluation form.

Diffuse Axonal Injuries (“DAI”)

Diffuse Axonal Injuries are another common brain injury resulting from automobile accidents. PCS and DAI are easily confused because they share the same symptoms, and there is no way to discern between the two. They may in fact be essentially the same condition. DAI may be an explanation for why PCS happens. Nevertheless, because the two are separated in the scientific literature, I discuss them separately.

DAI is trauma to the long thin extensions of neurons, which disrupts complex neural networks with devastating functional consequences but frequently without an abnormality on MRI or CT. Diffuse Axonal Injury can occur without any direct impact on the head, as it requires only the condition of rapid acceleration / deceleration such as takes place in whiplash injuries due to acceleration / deceleration resulting in rapid flexion-extension movement of the neck. It is not the contact phenomenon which causes DAI, but rather the change in momentum. Studies have found that 85.2% of all Diffuse Axonal Injuries are caused by motor vehicle accidents.

The brain is made up of many different layers of matter, each which have a different density from each other. When the brain is subjected to acceleration/deceleration forces, the different layers are accelerated/decelerated at different speeds. The most obvious differences in density of the brain are between the cerebral cortex (the gray matter) and the subcortical regions (the white matter.) As these different layers of the brain have different densities, and are located at varying distances from the center of the given rotation, they will be accelerated and decelerated at different speeds when a rapid acceleration / deceleration occurs. This results in different layers of the brain sliding across each other, which puts unnatural stress on the axons, which extend across these layers. A neuron, such as the one shown below, may stretch from the gray matter through the white matter, or out of the brain and into the brain stem or spinal cord.

When axons are torn or stretched as a result of the different layers moving at different speeds, this is called “shearing.” This shearing damage is microscopic. Unlike what typically occurs with an impact injury, where bleeding and swelling can often be seen on a CT or MRI, shear injury occurs at the cellular level, as a result of damage to the brain's central cell, the neuron. It is for this reason that conventional imaging techniques have little diagnostic value with such injuries.

While these injuries are microscopic in nature, their effects and long term consequences are significant. The majority of neurological sequels and vegetative states following severe head injury are thought to be due to DAI. 14, 26 More importantly, it is now well known by medical researchers that brain trauma in humans increases the risk for developing Alzheimer's Disease later in life. Diffuse Axonal Injury is the primary vector of Alzheimer's according to these researchers. “Such injury is enough to cause microscopic damage throughout the brain that, in turn, initiates a cascade of biochemical events that leads to the subsequent formation of Alzheimer's-like plaques.” Researchers have observed that damaged axons, caused by automobile accidents, produce a sticky substance called A-beta that sets the stage for the later development of Alzheimer-like plaques. In a report presented at the recent World Alzheimer Congress 2000, Steven T. DeKosky, MD, and colleagues at the University of Pittsburgh Medical Center reported findings from neocortical samples taken from brain injury patients one and three days after head injury showing that these changes had already started to take place.

Alzheimer's disease, the most common form of dementia in elderly people, is a progressive, degenerative brain disease that results in cognitive decline, impaired memory and thinking, behavior changes, loss of language, motor skills and a decline in the ability to perform basic activities. Head trauma expert John Q. Trojanowski, MD, PhD, Professor of Pathology and Laboratory Medicine at the University of Pennsylvania states that there is “very strong evidence that there is a connection between head trauma and at least some of the pathology of Alzheimer's disease.” In fact, the American Journal of Epidemiology noted that a person who sustained a head injury in a car accident were 350% more likely to get Alzheimer's that they were prior to the accident. Based on the strength of this research there is a greater than reasonable medical probability that people injured in a Motor Vehicle Collision have already started the development of Alzheimer's Disease as a result of their collision.

Lastly, a substantial amount of research has been done in this area which shows profound cognitive, behavioral, developmental, social and emotional damages to children injured in collisions. They need to be evaluated and treated where appropriate by a child psychologist and/or neurologist.

Where is the head injury located? Only a doctor, or neuropsychologist can tell. But, consider the following:

Frontal Lobe:

• 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:

• 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:

• 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:

• 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 catagorize objects (Categorization).
• Right lobe damage can cause persistent talking.
• Increased aggressive behavior.

Brain Stem:

• 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:

• 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.

If you have a traumatic brain injury case, you will need a lawyer who fully understands these conditions. Please feel free to call us today at (503) 227-1233 to set up your free consultation, or fill out our online case evaluation form.

Inner Ear Injuries & Perilymph Fistula

The inner ear is comprised of two main sections; the vestibular system and the cochlear system. The vestibular system is involved in balance, while the cochlea is involved in hearing.

The anatomy of the inner ear is dominated by large fluid-filled spaces. The inner ear consists of a complex series of tubes, running through the temporal bone of the skull. The bony tubes (sometimes called the bony labyrinth) are filled with a fluid called perilymph. Within this bony labyrinth is a second series of tubes made out of delicate cellular structures (called the membranous labyrinth). The fluid inside these membranous structures is called endolymph, The different spaces of both the perilymphatic and endolymphatic compartments are interconnected by a series of ducts.

An important feature of the endolymphatic space is that it is completely bounded by tissues and there are normally no ducts or open connections between perilymph and endolymph. These fluids are retained by the round and oval windows at the front wall of the inner ear.

The existence of the many ducts connecting different parts of the inner ear has led to the idea that the cochlear fluids are flowing through the ear. However, unlike other body fluids, such as saliva or lachrymal fluid (tears), the fluids of the inner ear are not secreted and resorbed in volume. This is a widespread misconception, based on old studies which used poor experimental techniques. Studies performed over the past decade have shown that neither endolymph nor perilymph “flow” along their respective compartments in the normal cochlea. Maintenance of the chemical composition of both fluids is dominated by ion transport processes which are localized in each region.

Now we turn to the effects of trauma on the inner ear.

In general terms, a perilymph fistula is an abnormal connection between the inner ear fluid spaces and the middle ear air spaces resulting in the leakage of perilymphatic fluid into the middle ear. Perilymph fistulas can be caused by trauma, and we deal with many clients who have sustained these injuries in a collision. Symptoms of perilymph fistula are variable and include sensorineural hearing loss, vertigo, dysequilibrium, unsteadiness, motion intolerance, and aural fullness. Many of these clients also have noise sensitivity (hyperacusis), tinnitus, memory loss, confusion, visual sensitivity and fatigue. Due to the several overlapping symptoms between this condition and mild traumatic brain injuries one really needs a consultation with a neurologist, and then either a neuropsychologist, a neuro-otologist or EENT specialist, or both, in order to differentiate the conditions. While advocates of both conditions believe their particular favorite is the cause of many of the similar symptoms, both camps seem to ignore that you could very well have both after trauma. As lawyers we wait to see where the testing shows the problems and then advocate for our clients on the actual injuries sustained.

These symptoms can be very dangerous to the injured person, if left untreated. Not only that, but there are some very good doctors who can work with you using conservative methods.

Clinically, the rupture of the oval or round window allows for the spilling of the inner ear fluid into the inner ear, where it either remains to irritate the patient, or goes down the Eustacian tube causing an itching sensation in the throat. The desire to clean one's ears frequently, the sensation of water in the ear when there could be none, and an itchy throat signaled by the injured person's regular throat noises (made in an attempt to “scratch” the itching sensation caused by the leak of fluid into the throat) are warning signs that you need to look for inner ear damage.

We are lucky enough to have several of the world's top experts in inner ear injuries in Portland. Several offices in the area are outfitted with a computer system which can simultaneously read the electrical activity in the leg, the eyes and the ears in reference to a person's recruitment to keep balance. This information then is compared to normals and a printout is obtained to determine the likelihood for Perilymph Fistula along with several other neuro-otological conditions.

The entire pressure gradient range of the inner ear is very small. As a result, the force created from a low speed impact is more than sufficient to cause a tear in either the oval or round window.

What few people know, or consider, is that the inner ear is connected to the subarachnoid space by the cochlear aqueduct. If the round window or oval window of the inner ear is perforated due to trauma, then perilymph escapes, driven by the hydrostatic pressure of Cerebral Spinal Fluid. The escaping perilymph and endolymph is replaced by CSF entering the cochlea through the cochlear aqueduct. In this condition a longitudinal flow will exist between the cochlear aqueduct and the site of the perforation. The chemical composition of perilymph will be disturbed because the perilymph will continually be “washed out” and replaced by CSF. This condition is what is technically known as a perilymphatic fistula.

This will also result in lower than normal CSF fluid levels in the brain and spinal cord. For this reason, the most common repercussion of this leak is a low grade headache, but it can certainly become more serious than this.

In addition to the aforementioned problems a perilymph fistula permanently alters the function of the postural muscles, in an attempt to recruit them to maintain balance. The tie between whiplash injuries, equilibrium problems and posture changes was noted in a 1997 study from Italy. The study also noted that the cervical problems compounded the equilibrium problems stating “it appears reasonable to assume that cervical proprioceptive alterations play a preminent role in the genesis of whiplash-induced chronic postural instability. This would result in an attempt to vary the physiology from an ankle to a hip strategy; incomplete manifestation of this new posture would cause the feeling of instability mentioned by the patients and documented by posturography.” P. Giacomini, A. Magrini, F. Sorace. Alterazioni della strategia posturale nel “colpo di frusta” valutate mediante posturografia statica. Acta Otorhinolaryngol Ital 17 (6), 409-413, 1997.

In short, neck injuries and perilymph fistulas together cause significant long term postural problems, and it is unlikely that either can be properly corrected without correction of the other. Moreover, this may explain why some patients do not properly heal from their spinal injuries, when there is a concurrent inner ear injury. From a proprioceptive standpoint these injured people are forced to alter their cervical position to remain upright.

The more significant repercussions of this problem are that people can not normally place themselves in space, leaving them susceptible to falls, bumping into objects, crashing into objects while driving in a car, and drowning if disoriented while underwater. Even more problematic though, is the potential for meningitis to spread from the inner ear during a routine upper respiratory infection.

There are conservative measures which are successful in many cases ranging from bed rest immediately after the collision for several weeks, to vestibular repositioning therapy called the “Epley Maneuver.” In cases where the ear does not heal conservatively, there is the option of surgery. There are several large studies reporting the results of surgical treatment of perilymphatic fistulas. The percentage of patients with fistulas found surgically ranges from 24% to 93%. Vestibular symptoms had the best response to surgical treatment, with 60% to 90% of cases improving. Hearing loss responded much less favorably except in fluctuating or progressive sensorineural hearing loss in which case surgery would often stabilize or slightly improve the hearing. Postoperative management consists of bed rest, head elevation and no straining for the first 5 days, followed by 4 to 6 weeks of light, non-strenuous activity.

If you have an inner ear injury case, you will need a lawyer who fully understands these conditions. Please feel free to call us today at (503) 227-1233 to set up your free consultation.