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Oregon Personal Injury Lawyer attends Brain Injury Alliance of Oregon Annual Conference

March 12, 2016  |  Brain Injury, General, Personal Injury, Resources  |  No Comments  |  Share

Oregon Personal Injury Lawyer Aaron DeShaw is attending the Brain Injury Alliance of Oregon Annual Conference this week.

The conference is a joint conference for Oregon, Washington and Idaho Brain Alliance organizations to bring together brain injury doctors (including MDs, DCs, DOs, neuro-opthomalagists), nurses, speech pathologists, neuro-cognitive rehabilitation specialists, biofeedback providers, auxiliary health care providers, long term care facilities, brain injury support group leaders, veteran affairs, brain injury survivors and family members, and a few brain injury lawyers.

While Dr. Aaron DeShaw is a full time lawyer at our firm, he attends most of the medical programs at the conference to ensure he fully understands the medicine and scientific literature of traumatic brain injuries.

Highlights of the conference involve OHSU Brain Injury Institute director Dr. James Chestnutt (on treatment of concussion in both hospital and cognitive rehabilitation settings), Rolf Gainer of the Neurologic Rehabilitation Institute and Brookhaven Hospital (on permanent cognitive and personality changes of people with traumatic brain injury) and the conference keynote speech by one of the nation’s leading neurologists Dr. Glen Zielinski (on the topic of traumatic brain injuries, post-TBI visual defects, and vestibular rehabilitation) including his successful treatment of people with significant traumatic brain injuries including quadriplegia as well as his work with world class snowboarder Kevin Pearce featured in the movie The Crash Reel.  (Pearce, who had been seen at The Craig Hospital in Colorado, but continued to have residual symptoms).

The annual conference provided great information about the breakthroughs that doctors are making in the detection and treatment of brain injuries.

Aaron DeShaw is a board member of the Brain Injury Alliance of Oregon.

Fleeting Blindness or Temporary Blindness after Trauma

01_dande_gOur law firm has experience representing people who have sustained temporary blindness (or sometimes called “Fleeting Blindness”) following an injury to the upper cervical spine in a motor vehicle collision.  Needless to say, it is a cause of great concern for people who lose sight temporarily after a traumatic injury.  While some of the clients have had multiple episodes of blindness lasting only 5-10 minutes, one client reported a 30 minute total loss of vision, and another client reported a 45 minute total loss of vision after a series of episodes of blindness lasting approximately 10 minutes.  While the insurers and defense doctors will claim this is purely psychological (often “conversion disorder”), we are aware of the actual physical injury causing this injury and are able to prove that at trial for people who have sustained blindness after trauma.

There are a number of emergency situations directly following a trauma to the head and/or neck including things like an artery dissection or an bleeding traumatic brain injury which should be checked out at an Emergency Room immediately.  But this discussion considers people who have these symptoms sometimes months after the injury, or on a repeated basis.

These clients have one thing in common.  They each sustain injuries to the ligaments of the upper neck, referred to as the Alar Ligaments, the Transverse Ligament and/or the Capsular ligaments at the Occiput (posterior skull) – C1- C2 region (often referred to as the Craniocervical Junction, or the Atlantoaxial region.)  The end result of damage to these structures (which support the skull on the neck) is that they leave the C1 vertebra unstable.  Instability of the C1 vertebra leaves the person particularly susceptible to a variety of symptoms given the compact and critical anatomy in that area of the body – namely the vertebral artery,  the Foramen Magnum, and the transition of the brain stem / spinal cord.

The full extent of symptoms arising from injuries to this area are beyond the scope of this article, but can include a feeling that the head feels unstable on the neck, dizziness with neck motion, and abnormal (and repeatable) clunking sound with movement of the head, other visual defects besides blindness (often tunnel vision or a “greying” out of vision), low grade headaches, and other symptoms.  [Injuries to this area also can cause a traumatic or Type II Chiari, causing abnormal pressure in the brain leading to different symptoms which are similarly difficult to diagnose.]

The temporary blindness and other temporary visual symptoms occurs due to an instability of the C1 vertebra leading to compression of the vertebral artery within the transverse foramen of the neck. The vertebral artery gets stressed and then compressed as C1 moves an abnormal amount, thereby shutting down blood flow from the vertebral artery into the brain.  This in turn shuts down the blood supply to the occipital lobe which processes visual information in the brain. This lack of blood flow results in the temporary blindness.

The injuries to the ligaments of the Craniocervical Junction and the resultant C1 instability are the subject of the new medical text “The Craniocervical Syndrome and MRI” published by Karger (2015).  The book features notable doctors studying this condition, including Raymond Damanian, inventor of the MRI machine.  At p.58 of the text, it notes “Misalignments of the CCJ [Craniocervical Junction] have been shown to contribute to vertebral artery insufficiency. Vertebrobasilar insufficiency or vertebral basilar ischemia refers to temporary symptoms due to decreased blood flow in the posterior circulation of the brain.” This includes the most posterior area of the brain, the occipital lobe, which controls the processing of visual information. Lack of blood to this area, results in temporary blindness.

Needless to say, this is a serious injury that should carry a substantial value in a personal injury claim. The only known method of correcting this instability is a fixation surgery of C1, a surgery which few neurosurgeons are willing to perform without a fracture of one of the cervical vertebra.  Which leaves people with these injuries the task of either finding a doctor willing to do the surgery or living with the symptoms for life.

Our firm has extensive history handling claims of C1 instability after trauma.  Dr. DeShaw has lectured both nationally and internationally to both doctors and lawyers on this topic.

If you have a case of temporary blindness after a traumatic brain or cervical spine injury, feel free to call our office for a free initial consultation at (503) 227-1233.

Post Concussion Syndrome Lawyer

September 29, 2015  |  Brain Injury, Personal Injury  |  No Comments  |  Share

pcsPost Concussion Syndrome, is a sequela of a traumatic brain injury (TBI). As you will note in this illustration, the brain suffers injury in instances when the head moves rapidly enough to allow the brain to move through its protective CSF fluid barrier, striking the inside bones of the cranium, even when the head itself does not strike an exterior object.  The mechanism in the far right images are called a “coup contrecoup” injury.

The commonly used medical text, 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, can be missed by doctors who are not adequately trained about standard definitions of Traumatic Brain Injury in place since the early 1990s. Since we deal with a large number of brain injuries, we have substantial experience handling as a post concussion syndrome lawyer. Based on the available medical research in this area, Dr. DeShaw has compiled a standard set of questions we ask every new client.  Doctors and other lawyers regularly refer people with traumatic brain injuries to our office. Over 90% of all our clients meet the diagnostic criteria for some variety of traumatic brain injury like Post Concussion Syndrome, an often debilitating brain injury.

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 Post Concussion Syndrome, or any other type of Traumatic Brain Injury is largely dependent upon the region of the brain injured in the accident.  Prior concussions can also lead to an increased risk of brain injury symptoms and an increased risk of permanent brain injury.  Contrary to the insurance company doctors’ opinions, even the United States Center For Disease Control and the National Institutes of Health have stated that 15% of people with mild traumatic brain injuries have permanent symptoms.

Post Concussion Syndrome can be challenging for some doctors because it requires time and work to diagnose it. 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.

In some cases (classified as “complicated mild traumatic brain injuries) high resolution 3T MRIs taken at 1mm slices can detect brain damage.  Diffusion Tensor Imaging or “DTI” can also detect some mild traumatic brain injuries.  In addition, researchers have been working on imaging to confirm the presence of mild traumatic brain injuries like Post Concussion Syndrome 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 Post Concussion Syndrome patients even if their initial Glasgow Coma Score was maximum (15).

If you have a traumatic brain injury case, you 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.

Diffuse Axonal Injuries in a Traumatic Brain Injury

June 29, 2015  |  Brain Injury, General, Personal Injury  |  No Comments  |  Share

It is now well accepted that all traumatic injuries involve both a mechanical and neurochemical changes within the brain.

Diffuse Axonal Injuries is the term used to explain the mechanical injury that results from a traumatic brain injuAxonal_Shearry.

Diffuse Axonal Injuries are the result mechanical trauma to the long thin extensions of neurons, which disrupts complex neural networks with devastating functional consequences but frequently do not show an abnormality on MRI or CT because the area of damage is too small to image. 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 motor vehicle crashes, due to acceleration / deceleration resulting in rapid flexion-extension movement of the head. 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 crashes.

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 axis of 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 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. In fact, CT and MRI are read as “normal” in nearly 100% of mild traumatic brain injuries.  This is particularly true when a standard resolution (1.5T) MRI is done with standard slice width (5mm).  The resolution of these imaging methods, and the width of the slices make it almost impossible to find microscopic areas of damage.  Despite this, autopsy studies demonstrate that MRIs and CTs miss nearly 100% of mild traumatic brain injuries, and also miss a high percentage of other injuries including small fractures and small internal bleeds.

While these injuries are microscopic in nature, their effects and long term consequences are significant. The majority of neurological sequela and vegetative states following severe head injury are thought to be due to DAI.   More importantly, it is now well known by medical researchers that brain trauma 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, 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.

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. Contrary to the insurance industry’s position that children are not injured in car accidents, and don’t require treatment, kids 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 symptoms that can arise with injuries to specific areas of the brain:

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).


  • 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.

The complex part of brain injuries is that axon injury in one part of the brain can impact functions in other parts of the brain because each axon can connect with thousands of others, which means all of those connections can be disrupted by damage to one very small area and certain skills are reliant upon cells in multiple areas of the brain.

If you have a traumatic brain injury case, you will need a Diffuse Axonal Injury lawyer who fully understands these injuries. Please feel free to call us today at (503) 227-1233 to set up your free consultation.

Traumatic Myasthenia Gravis Lawyer

Traumatic Myasthenia Gravis Lawyer

Our law firm is known for handling even the most complex neurological injury cases resulting from trauma. As this post discusses, we have experience handling a legal case in which Myasthenia Gravis was severely aggravated by an injury.

Myasthenia Gravis comes from the Greek and Latin words meaning “grave muscular weakness.”

Common symptoms of the condition can include:lrg273_183716MGDroop

  • A drooping eyelid
  • Blurred or double vision
  • Slurred speech
  • Difficulty chewing and swallowin
  • Weakness in the arms and legs
  • Chronic muscle fatigue
  • Weakness that comes on with activity, and improves following rest.
  • Difficulty breathing

The most common form of Myasthenia Gravis is an autoimmune condition of the nerve junctions.  The condition causes weakness of the voluntary muscle groups.   The condition is rate (approximately 20 in 100,000 Americans), and few doctors know much about it.  While some doctors will summarily reject the idea that an autoimmune condition can be caused or aggravated by trauma, the tie is now well established in the medical literature.

Why do people with Myasthenia Gravis get weak?  The voluntary muscles of the body are controlled by nerve impulses that arise in the brain. When the nerve impulses from the brain arrive at a nerve ending, it releases a chemical called acetylcholine. Acetylcholine travels across the space (called the neuromuscular junction) to the muscle fiber side, where it attaches to many receptor sites. A muscle contracts when enough of the receptor sites have been activated by acetylcholine. In Myasthenia Gravis, there can be up to an 80% reduction in the number of the receptor sites. The reduction in the number of acetocholine receptor sites is caused by an antibody that destroys or blocks the receptor site.  The autonomic nervous system and the GI tract (which are both known to be injured in traumatic injuries) control the immune system.  Normally the immune system makes antibodies to fight disease.  But, the immune system of the person with Myasthenia Gravis makes antibodies to fight against the receptor sites of the neuromuscular junction.  The abnormal function of the autonomic nervous system causes the body to attack itself.  Abnormal antibodies can be measured in the blood of many (but not all) people with MG. The antibodies destroy the receptor sites more rapidly than the body can replace them. Muscle weakness occurs when acetylcholine cannot activate enough receptor sites at the neuromuscular junction to contract the muscle normally.

This can progress to a life threatening state.  A myasthenic crisis occurs when the muscles that control breathing weaken to the point that ventilation is inadequate, creating a medical emergency and requiring a respirator for assisted ventilation. In individuals whose respiratory muscles are weak, the myasthenia crisis can be triggered by infection, fever, or an adverse reaction to medication.

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. One of 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.  Another article of onset of Myasthenia Gravis after trauma can be found here.

But, the case for aggravation due to trauma and medical treatment for that trauma, 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 slight 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 between two large vehicles, our client was subjected to a series of treatments known to be 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 for onset of Myasthenia Gravis as a direct result of the collision, triggering a severe aggravation of the condition. This aggravation took her from having non-symptomatic myasthenia gravis with negative lab tests, to being housebound and having myasthenic crises which required lifetime home care and repeated hospitalizations for a woman who was previously completely healthy and independent. Other cases of post traumatic Myasthenia Gravis have been reported at Johns Hopkins Medical School.

It is because of our experience handling exceptionally complex injury cases that we have become the lawyer of choice for people with traumatic brain injuries, spinal cord injuries, and other serious neurological injuries.  If you have experienced the onset or worsening of Myasthenia Gravis after an injury, and would like to retain an experienced Myasthenia Gravis lawyer to assist you in the matter, either as your primary law firm, or as co-counsel, please contact us at (503) 227-1233.