Pediatric brain injuries result in more than $1 billion in hospital charges annually. The most dangerous age groups, statistically, are children from 0 – 4 years-old, and children from 15 – 19 years-old.

The most common causes of pediatric TBI are as follows:

• Car Accidents
• Falls
• Assaults
• Sports and Recreational Activities
• Child Abuse

While the acute symptoms of pediatric TBI are similar to the acute symptoms of adult TBI, unfortunately, pediatric TBI can result in significant long-term functional problems. It is important that children’s brains are not thought of as miniature adult brains. It has long been thought that brain injuries to children were not as serious because their brains could essentially rewire themselves to overcome any brain damage. Long term studies have shown that this neuroplasticity theory is not accurate.

Studies have also shown that following a pediatric TBI, children go through an immediate phase of recovery, but then they typically experience a decline and then a Neurocognitive Stall that results in symptoms plateauing, as opposed to improving.

It is critical that pediatricians recognize the long-term consequences involved in pediatric TBI, so children can be monitored at each stage of their neuro-cognitive development in order to determine if they are falling behind in any particular area of development.

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Contact an experienced Pediatric TBI Attorney.

The difference between images shown on the newest DTI scans vs. the images shown by HDFT in the new study are striking. DTI collects data points from 51 directions, while HDFT collects data points from 257 directions. Essentially, HDFT is 5 times more detailed than DTI, which is very exciting considering that DTI detected some type of abnormality in nearly all of my TBI  clients.

HDFT holds the potential to legitimatize the complaints of TBI survivors that are typically ignored by emergency personnel and general practitioners. The new imaging technique may also put an end to the ridiculous and dangerous position taken by the neurologists and neuropsychologists working for the insurance industry that claim mild traumatic brain injuries cannot result on permanent ongoing problems. No longer will TBI survivors be neglected because they suffer from invisible injuries.

The study was funded by the Defense Advanced Research Projects Agency. Other medical centers and military hospitals will begin implementing studies regarding HDFT in the next six months and the Pitt researchers are optimistic that HDFC could become a routine imaging technique for TBI patients within the next 5 to 10 years.

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Contact Attorney Randy Rozek, an Experienced Wisconsin Traumatic Brain Injury Attorney.

There are several different medical diagnoses concerning changes in the ability to smell and taste, including the following:

SMELL

• Anosmia – a complete loss of sense of smell
• Hyposmia – a diminished sense of smell
• Parosmia – a change or alteration in the sense of smell

TASTE

• Ageusia – a complete loss of sense of taste
• Hypogeusia – a partial loss of sense of taste
• Dysgeusia – a change or alteration in the sense of taste

The ability to taste certain types of food is closely linked to the ability to smell, so often the change in sense of smell results in a change in the ability to fully taste everything.

Importantly, it is not the injury to the brain itself that causes the change in the ability to smell or taste, instead it is typically separate damage to the Olfactory Bulb that results in the change in smell or taste. The Olfactory Nerves carry information from the nose to the brain. Unfortunately, it must travel into the skull in an area with rough, sharp ridges called the Cribriform Plate, which makes the Olfactory Nerves very susceptible to trauma. (See Diagram to the Right). In an accident, if there is enough force to cause a brain injury, then there certainly will also be enough force to cause damage to the Olfactory Nerves and/or Olfactory Bulb.

Changes in the sense of smell are usually detected through the administration of a Smell Test. While there are a variety of different Smell Tests, the most common is the University of Pennsylvania Smell Identification Test or UPSIT, which was invented by Richard Doty, PhD, a pioneering researcher in the loss of sense of smell. The UPSIT is essentially a scratch and smell test of 40 items. The test can be self-administered, it can detect if someone is not being accurate regarding their loss of smell and it is also normed for age, gender, smoking habits, and a wide variety of olfactory disorders.

Unfortunately, in my experience representing brain injury survivors, I have found that doctors and neuropsychologists rarely even ask their patients if they have noticed a change in their ability to smell or taste, let alone administer a valid smell or taste test. TBI survivors that have noticed changes in their sense of smell or taste must bring it to their doctors attention. They should be referred to an ENT for administration of a valid Smell Test and to explore potential treatment options, which can include zinc supplements, medications or possibly even surgery. Unfortunately, post-traumatic Anosmia and/or Ageusia is usually not curable.

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Contact Attorney Randy Rozek, an Experienced Wisconsin Traumatic Brain Injury Attorney.

Green Bay Hilton Garden Inn

As news surfaced of yet another carbon monoxide poisoning at a Green Bay hotel, it shed light on the reluctance of the hotel industry to address a major safety concern. On December 30, 2011, as many as 16 people were hospitalized after being exposed to dangerous levels of carbon monoxide while staying at the Green Bay Hilton Garden, 1015 Lombardi Ave., Green Bay, Wisconsin. The Green Bay Fire Department recently released their records that indicate four small children and several other people were suffering from common symptoms of carbon monoxide exposure, including vomiting, nausea and headaches.

The Green Bay Fire Department detected dangerous levels of carbon monoxide in several areas within the hotel, including the swimming pool area, the workout room, two restrooms and a stairway. Apparently the carbon monoxide level in the swimming pool area was a 800 parts per million (ppm) and 957 ppm in the pool equipment room. Buildings are typically evacuated at 9 ppm. Sustained exposure to carbon monoxide at levels as high as 800 ppm can be lethal. Carbon monoxide exposure can also result in severe long-term consequences, such as brain injury and heart problems. The Hilton Garden Inn general manager, Michelle Lang, has continued to remain silent as to how this could have happened to their guests.

Green Bay Hilton Garden Inn Swimming Pool

The hotel industry has long recognized the dangers of carbon monoxide exposure, yet some hotel chains have failed to institute uniform policies requiring the installation of carbon monoxide detectors throughout their hotels. Ironically, exactly one year prior to the date of the Green Bay Hilton Inn carbon monoxide poisoning incident, our office joined forces with the Brain Injury Law Group to file suit on behalf of victims who were poisoned by carbon monoxide while staying at the Green Bay Day’s Inn back in May of 2009. Now 2 1/2 years later, it is apparent that some hotel chains have still done nothing to protect their guests from carbon monoxide exposure, like simply installing working carbon monoxide detectors. Under Wisconsin Safe Place Law, hotel owners are required to keep their hotels as “free from danger to the life, health, safety, and welfare of guests as the nature of the hotel will reasonably permit.” The failure to install carbon monoxide detectors throughout a hotel clearly violates this law and until the hotel industry gets this message loud and clear, hotel guests throughout the world will continue to get sick and even die from carbon monoxide poisoning.

Chronic Traumatic Encephalopathy is a progressive disease that results in a gradual decline in cognitive function. Victims of Chronic Traumatic Encephalopathy exhibit symptoms consistent with dementia, including confusion, memory loss, depression, and aggressive behavior. The hallmark indicator of Chronic Traumatic Encephalopathy on autopsy of the brain was the buildup of a plaque referred to as tau protein. While it was always understand that repeated concussions could result in the buildup of tau protein, it wasn’t until recently that researchers were able to identify the buildup of tau protein in individuals with only a single head injury. (Victoria E. Johnson, William Stewart, Douglas H. Smith. Widespread Tau and Amyloid-Beta Pathology Many Years After a Single Traumatic Brain Injury in Humans. Brain Pathology, 2011; DOI: 10.1111/j.1750-3639.2011.00513.x).

Alzheimer’s Disease is a progressive form of dementia. It is the most common type of dementia, resulting in confusion, anger outbursts, lack of long-term memory, and language deficits. The cost of Alzhiemer’s Disease on society is great. Because most Alzheimer’s patients will continually and progressively decline, at some point they will have to rely upon others for their care. While family members and loved ones usually try to provide care initially, the challenges of caring for an Alzheimer’s sufferer can take an incredible toll on every aspect of a caregiver’s life. What makes it additionally challenging and unrewarding is that, at some point, the Alzheimer’s sufferer will no longer have the long-term memory required to remember the identity of their caregiver. On autopsy it has been show that tau protein buildup is also a hallmark indicator of patients with Alzheimer’s Disease. Studies have shown that brain injury victims have an increased risk of developing Alzheimer’s Disease.

Parkinson’s Disease is a progressive disorder of the central nervous system with its origins in the midbrain. The initial symptoms of Parkinson’s Disease involve movement disorders, but later Parkinson’s Disease patients typically develop cognitive symptoms including dementia. Parkinson’s Disease, while typically idiopathic in origin, can follow traumatic brain injury that results in damage to the basal ganglia which can result in a dopamine production disruption. (Traumatic Brain Injury in Adult Rats Causes Progressive Nigrostriatal Dopaminergic Cell Loss and Enhanced Vulnerability to the Pesticide Paraquat Che Brown Hutson, Carlos R. Lazo, Farzad Mortazavi, Christopher C. Giza, David Hovda, and Marie-Francoise Chesselet Journal of Neurotrauma 2011 28:9, 1783-1801). Unfortunately, there is no lab test to definitively diagnose Parkinson’s Disease as of yet. Due to the degenerative nature of Parkinson’s Disease, patients and their loved ones face an enormous burden when dealing with long-term care for the Parkinson’s patient.

As if traumatic brain injury survivors did not have enough to deal with just attempting to recover from their injury, now studies have established that victims of TBI have an increased risk of developing early onset dementia, Chronic Traumatic Encephalopathy, Alzheimer’s Disease, and Parkinson’s Disease.