Frequently Asked Questions

Answers provided by:
Robert Katz, Ph.D. (RK)
Jennifer McCain, Psy.D Neuropsychologist (JM)
Syed Rahman, M.D. (SR)
Noreen Bock, CSW (NB)

Part 3

Traumatic Brain Injury (TBI) is defined as sudden, permanent damage to the brain caused by external, mechanical forces (e.g., a blow to the head suffered during a motor vehicle accident). Thus, there is a clear distinction between TBI and brain injury caused by internal events (e.g., stroke, anoxia, tumor), developmental disabilities (e.g., mental retardation, cerebral palsy, autism), and progressive illnesses such as Alzheimer's Disease and Parkinson's Disease. When a TBI occurs, the brain may be penetrated from the outside, as in the case of a gunshot wound (open head injury), or not (closed head injury). The term head injury is often also used to refer to TBI as well as to internal brain events such as anoxia (lack of oxygen to the brain due to cardiac arrest or cessation of breathing from other trauma), stroke (disruption in the blood supply to the brain due to either blockage or hemorrhage of one more blood vessels in the brain), tumor (a mass of new tissue), or encephalopathy (inflammation of the brain). (RK)

Any head injury can cause disruption of brain functions and can result in physical, cognitive, and psychosocial/emotional/interpersonaI impairment. Strokes often cause physical deficits such as hemiplegia (weakness or even paralysis on the side of the body opposite the side of the brain effected by the stroke), dysarthria, (problems with speech production due to deficits in speech apparatus coordination), ataxia (motor coordination problems), and apraxia (difficulty with purposeful, voluntary muscle movements in the absence of paralysis or paresis), decreased arousal (hypoarousal), changes in mood (especially depression) and emotional control, impulsivity, memory deficits, concentration problems, visual inattention (neglect) of the affected side, language deficits causing communication problems (aphasia) when the stroke is on the left side of the brain, and visuoperceptual problems when the stroke is on the right side of the brain.

Anoxia can cause significant impairment of learning, memory, judgment, mental flexibility, and can even result in behavioral changes and regressed behaviors when the injury is severe. Tumors lead to specific deficits; any function can be impaired, depending on the location of the tumor in the brain.

TBI differs from other types of head injuries in that while the brain damage from tumors, strokes, anoxia, etc., is likely to be confined to one area of the brain, TBI (closed head injury) often results in brain damage which is widespread or diffuse, resulting in many different impairments.

Physical deficits from TBI often include sensory-motor deficits (e.g., loss of smell, taste, balance, tactile sensation), motor control and coordination problems (e.g., ataxia, dysarthria), fatigue, seizure disorder or epilepsy, decreased tolerance for drugs and alcohol, and headaches.

Cognitive deficits include memory and learning impairment, attention/concentration problems, arousal deficits, slowed mental processing, psychomotor retardation, executive function impairment (deficiencies in planning, organization, problem solving, judgment, abstract reasoning, sequencing, mental flexibility, shifting mental set), visuoperceptual-motor deficits, eye-hand incoordination, language and communication disorders such as aphasia, reading comprehension impairment, initiation problems, and decreased general intellectual functioning.

Psychosocial/emotional/interpersonaI deficits from TBI include loss of emotional control (disinhibition), impulsivity, problems with anger management, impatience, irritability, uncooperativeness, anxiety, adynamia (severely reduced initiative), passivity, apathy, withdrawal, interpersonal and conversational skill deficits, social inappropriateness, self-regulation problems, unrealistic expectations, psychiatric disorders (e.g., depression, psychosis, substance abuse), inability to profit from s.htback or experience, and reduced self-awareness and insight. (RK)

A head injury will frequently impact on the survivor's initial level of consciousness. Level of consciousness is a continuum ranging from full alertness, drowsiness, lethargy, daze-like symptoms, to loss of consciousness or coma. Loss of consciousness typically involves injuries to the brain stem, the oldest part of the brain, which is responsible for basic fife functions such as alertness, arousal, heartbeat, and breathing.

It is rare for true coma to last more than several weeks, and in fact, almost all survivors will eventually awaken from a coma. The length of time before someone wakes up depends on the severity of the injury. It is important to understand that emergence from a coma is a gradual process in which the brain injured survivor may go through several stages including periods of disorientation, post-traumatic or anterograde amnesia (survivor has no memory of recent events), agitation. Some of these survivors may require medication or even physical restraints to prevent them from harming themselves or others. (RK)

A survivor's degree of consciousness is often used to determine the severity of his/her brain injury. Instruments such as the Glasgow Coma Scale (GCS) use the survivor's visual, motor, and verbal responsiveness to measure level of consciousness. A copy of the GCS can be found in our Glossary section. Scores of 8 or below are considered to represent a true coma (no eye opening, no response to simple commands, and unable to communicate) and to indicate a severe brain injury. Scores from 9 - 12 on the GCS are suggestive of a moderate brain injury. GCS scores of 13 and above are thought to indicate that the brain injury is mild.

The duration or length of coma (LOC) is also used to measure severity of injury and to predict outcome. The longer the LOC, the more severe the brain injury. LOC greater than 6 hours post-admission is considered to be a severe brain injury. LOC between 20 minutes and 6 hours post-admission is considered to be moderate brain injury. LOC of less than 20 minutes is considered to be indicative of a mild brain injury. (RK)

The extent of survivor recovery is based on the severity of the head injury. The more severe the injury, the greater the liklihood that the survivor will be unable to reach his/her preinjury level of functioning. Significant others will need to be patient because the magnitude of recovery may not be known for some time. Most researchers believe that meaningful spontaneous (natural) recovery is possible 1 -to 2-years postinjury. In addition, there are many studies demonstrating the neuropsychological rehabilitation can improve recovery many years after a head injury. (RK)

The following are the main factors that have been found to predict long-term outcome for head injured survivors:

(a) Severity of cognitive deficits including memory and learning impairment, attention/concentration problems, arousal deficits, slowed mental processing, psychomotor retardation, executive function impairment (e.g., deficiencies in planning, organization, problem solving, judgment, abstract reasoning, sequencing, mental flexibility, and shifting mental set), visuoperceptual-motor deficits, eye-hand incoordination, language and communication disorders such as aphasia, reading comprehension impairment, initiation problems, and decreased general intellectual functioning.

(b) Severity of psychosocial/emotional/interpersonaI deficits including loss of emotional control (disinhibition), impulsivity, problems with anger management, impatience, irritability, uncooperativeness, anxiety, adynamia (severely reduced initiative), passivity, apathy, withdrawal, interpersonal and conversational skill deficits, social inappropriateness, self-regulation problems, unrealistic expectations, psychiatric disorders (e.g., depression, psychosis, substance abuse), inability to profit from feedback or experience, and reduced self-awareness and insight.

(c) Severity of injury as measured by the Glasgow Coma Scale (see above), length of coma (see above), length of post-traumatic or anterograde amnesia (PTA) (survivor has no memory of recent events), total brain volume loss, and neuroimaging (e.g., CT Scan, NMI) has been shown to influence outcome. For example, severe TBI survivors experience higher unemployment rates than mild and moderate TBI survivors. However, more recently, the value of PTA, GCS, and LOC as predictors of long-term outcome for TBI survivors has been questioned.

(d) Pretrauma variables such as age at the moment of injury (TBI survivors over the age of 40 appear to have worse outcome than younger survivors), gender (there is some evidence for a differential effect from severity of brain damage on the sexes, with severe TBI samples showing a better outcome for women, and less severe samples showing a better outcome for men), and pretrauma education (while generally believed that the number of years of pretrauma education does not appear to affect postinjury outcome, there is some evidence that survivors with less than a high school education may have a worse outcome).

(e) Posttrauma environmental variables such as duration of vocational rehabilitation and community re-integration services (greater length of treatment associated with better outcomes), presence of a case manager for post-rehabilitation survivors (better outcome) and ,length of time since vocational rehabilitation program discharge (greater time since discharge associated with decreased outcome).

(f) Posttrauma substance abuse has also been associated with a decreased outcome.

In general, the TBI literature suggests that the cognitive and psychosocial/emotional/interpersonaI deficits associated with TBI exceed residual physical deficits and other factors as predictors of TBI outcome. (RK)

In my TBI outcome research, I found that an index measuring the degree to which head injured survivors were using the compensatory strategies which had been taught in their TBI rehabilitation program was the best predictor of long-term outcome. This finding validates the importance and effectiveness of teaching compensatory mechanisms in rehabilitation programs and suggests that most survivors could benefit from going through programs such as the Outpatient Rehabilitation Program here at Jamaica Hospital Medical Center (718-206-7140). I also found a negative relationship between length of time since discharge from rehabilitation program and compensatory strategy usage, which seems to indicate a need for periodic postprogram follow-up sessions to reinforce the usage of compensatory mechanisms.

Of most importance to the caregivers of TBI survivors however, was my finding that regardless of severity of injury, TBI survivors who were not living with family and had less family involvement were more independent with regard to home responsibilities than survivors with more family involvement. This finding suggests that rehabilitation programs should encourage family members of TBI survivors to carefully review the level of support which they are providing. For instance, they should consider whether and why they may be providing more assistance than is necessary or healthy for the survivors. Optimally, this exploration would take place in a nonconfrontational, therapeutic environment such as a family support group or a family therapy session, such as the ones provided here in the Outpatient Rehabilitation Program at Jamaica Hospital Medical Center (718-206-7140). The goals of these sessions should be to help families determine when it may be beneficial to push survivors toward more independent functioning and living, as well as to assist them in understanding the types of support which are most helpful in various situations.

Other interesting findings came out this study. Although the survivors denied using marijuana or other illegal drugs, the participants reported significant alcohol usage. This suggests that substance abuse counseling should be a significant focus of rehabilitation efforts. The Jamaica Hospital Medical Center Outpatient Rehabilitation Program (718-206-7140) can provide this treatment for head injured survivors.

Given that these cognitive rehabilitation and family therapy sessions might lead to an increase in referrals to programs which promote independent living for TBI survivors (e.g., transitional housing, independent living centers, supported apartment programs, halfway houses), the importance of allocating government funds for these programs becomes clear. In fact, you may notice that funding for all of the programs which I have suggested is limited at this point. Therefore, I strongly recommend that you get involved with the Brain Injury Association and the other advocacy groups which are listed in our web site and lobby for increased funding for outpatient, community-based programs for TBI survivors. (RK)

References for FAQ - Part 1 (RK)

Corthell, D. W. (1990). Traumatic brain injury and vocational rehabilitation. Menomonee, WI: The Research and Training Center, University of Wisconsin-Stout.

DeBoskey, D. S. (1996). Coming home: A discharge manual for families of persons with a brain injury. Houston, TX HDI Publishers.

Katz, R. A., Kay, T. E., & Keitel, M. A. (1998). The relationships among social support, autonomy, and vocational outcome following a traumatic brain injury. Rehabilitation Psychology 43(2).

Lezak, M. D. (1995). Neuropsychological Assessment (Third Edition). New York: Oxford University Press.

Williams, J. M., & Kay, T. (1991). Head injury: A family matter. Baltimore, MD: Paul H, Brookes Publishing Co.

Brain swelling or edema is one of the types of 'what we call secondary, mechanisms of brain damage, which commonly occur following an acquired brain injury. While the primary mechanisms of damage occur immediately at the moment of the injury, secondary mechanisms of damage tend to occur later and may be due to bleeding from damaged blood vessels (hemorrhage), and/or increased pressure within the brain (intracranial pressure) as the brain swells with fluid (edema or hydrocephalus) or blood. Secondary damage occurs more commonly after a severe brain injury. The further damage to the brain can be quite significant due to hypoxia (tissue death due to loss of oxygen) or herniation (squeezing out of brain tissue through small openings), and surgery may be necessary to stop the bleeding, remove clots, relieve pressure and/or swelling. (RK)

WHAT IS BRAIN DEATH?

Brain death is an irreversible type of unconsciousness distinguished by a total loss of brain functioning while the heart continues beating. While the legal definition for brain death differs between states, the typical clinical guidelines include the absence of reflex activity, movements, and respiration, dilated and fixed pupils, and electrical activity of the brain absent on two electroencephalograms (EEG) performed 12 to 24 hours apart. (RK)

A coma is a state of deep unconsciousness where the person cannot by aroused. It is generally characterized by the absence of spontaneous eye movements, response to painful stimuli, and vocalization. Loss of consciousness typically involves injuries to the brain stem, the oldest part of the brain, which is responsible for basic life functions such as alertness, arousal, heartbeat, and breathing.

A patient's degree of consciousness is often used to determine the severity of his/her brain injury. Instruments such as the Glasgow Coma Scale (GCS) use the patient's visual, motor, and IL verbal responsiveness to measure level of consciousness. Scores of 8 or below are considered to represent a true coma (no eye opening, no response to simple commands, and unable to communicate) and to indicate a severe brain injury. However, it is important to note that many medical professionals adhere to a broader definition of coma. Thus, patients who may have their eyes open some of the time and even stare and look around at times, may be still be referred to as being in coma if they can't communicate or follow commands. Scores from 9 - 12 on the GCS are suggestive of a moderate brain injury. GCS scores of 13 and above are thought to indicate that the brain injury is mild.

The duration or length of coma (LOC) is also used to measure severity of injury and to predict outcome. The longer the LOC, the more severe the brain injury. LOC greater than 6 hours post-admission is considered to be a severe brain injury. LOC between 20 minutes and 6 hours post-admission is considered to be moderate brain injury. LOC of less than 20 minutes is considered to be indicative of a mild brain injury.

The general misunderstanding of the definition of true coma can often interfere with the measurement of LOC. It is rare for true coma to last more than several weeks, and in fact, almost all patients will eventually awaken from a coma. However, it is important to understand that emergence from a coma is a gradual process in which the brain injured patient may go through several stages including periods of disorientation, post-traumatic or anterograde amnesia (patient has no memory of recent events), agitation. Some of these patients may require medication or even physical restraints to prevent them from harming themselves or others. The Rancho Los Amigos Scale is a commonly used instrument to record the stage of emergence from coma. (RK)

At present, we do not know whether a patient in a coma can feel pain or whether they can hear what we are saying, We do know however, that some studies have shown that coma stimulation, the process of providing sensory stimulation to coma patients including familiar stimuli such as familiar voices and music, has been shown in some studies to improve coma recovery. Thus, at the Brady Institute for Traumatic Brain Injury and Coma Recovery at Jamaica Hospital Medical Center (718-741-7824), we have developed the Brady Scale, a hierarchical interdisciplinary tool designed to monitor and guide coma recovery in each of the five sensory modalities (tactile, auditory, visual, gustatory, olfactory). The Brady Scale is administered to each coma recovery patient twice per day by the interdisciplinary treatment team. Based on the hierarchical level achieved by the patient on the Brady Scale, the patient's personalized coma stimulation program is amended daily to account for patient progress. The use of the Brady Scale has improved the ability to provide optimal Arousal to Unit coma recovery patients. (RK)

References - Part 2 (RK)

Mosby"s pocket dictionary of medicine. nursing, & allied health. (1994). St. Louis, MI: Mosby-Year Book, Inc.

Corthell, D. W. (1990). Traumatic brain injury and vocational rehabilitation. Menomonee, WI: The Research and Training Center, University of Wisconsin- Stout.

DeBoskey, D. S. (1996). Coming home: A discharge manual for families of persons with a brain injury. Houston, TX HDI Publishers.

Lezak, A D. (1995). Neuropsychological Assessment (Third Edition). New York: Oxford University Press.

Williams, I M., & Kay, T. (199 1). Head injury: A family matter. Baltimore, MD: Paul H. Brookes Publishing Co.

Usually seizure medications are tapered after 1 week of therapy except in the following: 

1. Penetrating brain injury 
2. Development of posttraumatic seizure. 
3. Prior seizure history. 
4. Patients undergoing craniotomy.

For patients in whom seizure medications are continued for any of the reasons above maintain 6-12 months of therapeutic levels. (SR)

What is Post Traumatic Amnesia:

Even after a fairly minor head injury there will be a time after the head injured person has apparently woken up, which he / she will, later be unable to remember. This time can range from a few seconds or minutes to days, weeks or months. During this period he may answer or ask questions, he may walk around, have a meal or do other apparently awake things, but because he or she is completely unable to remember them later, we know that he or she was obviously not actually awake. Post traumatic amnesia is basically the time between the injury and the resumption of normal continuous memory. (SR)

There are three cardinal neuropathologic dimensions that are considered in the diagnosis. They are the a) distribution b) severity and c) types of pathology.

Focal Lesions: severity factors depend on location size (bigger lesions worse than small), depth (deep lesions worse than superficial). The pathologic process  may involves hemorrhage, infarct, tumor, abscess, trauma and secondary effects (edema, mass effect, neuronal degeneration.

Multifocal Lesions: severity depends on factors same as that for focal lesions. In addition it also depends on number (the more lesions the worse), simultaneous Vs stages (simultaneous the worse) and unilateral Vs bilateral (bilateral worse). The pathologic process commonly involved are grossly same as that for focal lesions.

Diffuse Lesions : severity factors depend on density or quantity (the more the worse) , locations ( structures and neural elements involved ). The pathologic processes involved here are traumatic hypoxic, ischemic, inflammatory, metabolic, as well as degenerative secondary processes.

More over it has been known for a long time that when particular areas of brain are damaged there are characteristic effects on its function. For instance damage to the side of the brain half way from the front to the back (parietal area ) results in weakness of the arm or leg on the opposite side. Damage to the left side tends to impair speech. Injury behind the forehead ( frontal area ) results in changes in behavior and loss of restraint and insight. When there is localized injury to the brain perhaps caused by an open or penetrating injury, only one of these functions may be affected. However most head injuries are closed injuries caused by acceleration with multiple areas of brain damaged. Some or perhaps many of brain functions may be affected, some more severely than others. (SR)

It is likely that most of the brain cells which have been damaged will not get back to useful work. The majority of improvement that is seen after a head injury is due to reorganization of the brain undamaged. Using the large reserves of brain function that we all  have, intact areas take over from those that are no longer functional. Obviously if these reserves of brain have been reduced by previous injuries, or by the natural loss of nerve cells with age, recovery will be less complete. (SR)

When the patient is asleep after a head injury is called coma or unconscious. Both mean the same thing but the coma description is the more usual. It may take days or weeks to move out of coma stage into a less coma stage. The patient rarely moves abruptly from being in a coma to being properly awake. When the patient first starts to take notice of things around him, he or she is likely to be quite confused about where and why. The  patient at this stage is likely to ask you again and again what happened to him or her. At this stage the patient is starting to wake up, but still not able to remember things that have happened probably from one minute to the next. This stage is also where the patient is confused, repeats himself, and forgets things.  This might last for a short time only, for days, weeks or months. Usually the confused stage lasts longer the longer the period of coma has been. These two after effects of head injury, coma and period of confusion are used as one of the ways of describing the severity of the injury. In general the longer the person has been unconscious and the deeper the stage of coma at the time of admission, more badly the hurt is. Obviously the worse the injury is the longer the patient is going to take to recover. Almost without exception one can be sure that the patient will be better sometime in the future, but how much better is another matter and may depend on:

1. Severity of the injury. 
2. Whether there is further brain damage. 
3. Minimizing stress. 
4. Effective Rehabilitation 
5. Management of returns to school or work.

What Are Some Disabilities Connected With Traumatic Brain Injury?

Any head injury can cause disruption of brain functions and can result in physical, cognitive, and psychosocial/emotional/interpersonaI disability. Strokes often cause physical disabilities such as hemiplegia (weakness or even paralysis on the side of the body opposite the side of the brain effected by the stroke), dysarthria (problems with speech production due to deficits in speech apparatus coordination), ataxia (motor coordination problems), and apraxia (difficulty with purposeful, voluntary muscle movements in the absence of paralysis or paresis), decreased arrousal (hypoarrousal), changes in mood (especially depression) and emotional control, impulsivity, memory deficits, concentration problems, visual inattention (neglect) of the affected side, language deficits causing communication problems (aphasia) when the stroke is on the left side of the brain, and visuoperceptual problems when the stroke is on the right side of the brain.

Anoxia can cause significant impairment of learning, memory, judgment, mental flexibility, and can even result in behavioral changes and regressed behaviors when the injury is severe. Tumors lead to specific deficits; any function can be impaired, depending on the location of the tumor in the brain.

TBI differs from other types of head injuries in that while the brain damage from tumors, strokes, anoxia, etc., is likely to be confined to one area of the brain, TBI (closed head injury) often results in brain damage which is widespread or diffuse, resulting in many different impairments.

Physical disabilities from TBI often include sensory-motor deficits (e.g., loss of smell, taste, balance, tactile sensation), motor control and coordination problems (e.g., ataxia, dysarthria), fatigue, seizure disorder or epilepsy, decreased tolerance for drugs and alcohol, and headaches.

Cognitive disabilities include memory and learning impairment, attention/concentration problems, arousal deficits, slowed mental processing, psychomotor retardation, executive function impairment (deficiencies in planning, organization, problem solving, judgment, abstract reasoning, sequencing, mental flexibility, shifting mental set), visuoperceptual-motor deficits, eye-hand incoordination, language and communication disorders such as aphasia, reading comprehension impairment, initiation problems, and decreased general intellectual functioning.

Psychosocial/emotional/interpersonaI disabilities from TBI include loss of emotional control (disinhibition), impulsivity, problems with anger management, impatience, irritability, uncooperativeness, anxiety, adynamia (severely reduced initiative), passivity, apathy, withdrawal, interpersonal and conversational skill deficits, social inappropriateness, selfregulation problems, unrealistic expectations, psychiatric disorders (e.g., depression, psychosis, substance abuse), inability to profit from feedback or experience, and reduced self-awareness and insight.(RK)

Who Can Sustain TBI?

Anyone can sustain a TBI. However, of the 320,000 to 600,000 people who receive a TBI each year, over 60% of these are males under the age of TBI, the majority falling between the ages of 19 and 25 at the time of injury. The average age of a TBI survivor at time of injury is believed to be 22, with males outnumbering females by four to one. However, there are a significant number of persons who sustain a TBI in childhood and adolescence. TBI is the leading killer and cause of disability in children and young adults. Elderly persons also can receive a TBI; most of these are due to falls or elder abuse.

Aside for high-crime urban areas where assaults predominate, about one half (48%) of TBI's are caused by motor vehicle accidents. Other major causes of TBI include falls (2 1 %), non-firearm assaults (12%), sports/recreational activities (10%), and firearms (6%). In addition, substance abuse appears to be major contributing factor in over 50% of head injuries sustained in the United States. For example, Rimel and Jane (1983) found that 52% of their sample of head injured survivors were legally intoxicated at the time of injury, and 29% had previously received  substance abuse treatment. (RK)

How Is TBI Documented?

When the patient is brought to the emergency room for examination, a patient's degree of consciousness is often used to determine the severity of his/her brain injury. Instruments such as the Glasgow Coma Scale (GCS) use the patient's ocular, motor, and verbal responsiveness to measure level of consciousness. Scores of 8 or below are considered to represent a true coma (no eye opening, no response to simple commands, and unable to communicate) and to indicate a severe brain injury. Scores from 9 - 12 are suggestive of a moderate brain injury. GCS scores of 13 and above are thought to indicate that the brain injury is mild.

The duration of coma (LOC) is also used to measure severity of injury and to predict outcome. The longer the LOC, the more severe the brain injury. LOC greater than 6 hours postadmission is considered to be a severe brain injury. LOC between 20 minutes and 6 hours postadmission is considered to be moderate brain injury. LOC of less than 20 minutes is considered to be indicative of a mild brain injury.

At this time, diagnostic tests may be run to determine the extent of brain damage. The most common of these is the CAT (Computerized Axial Tomography) or CT scan, an x-ray technique that produces a cross sectional image of the brain. The CT scan is very useful in the early stages for detecting gross structural changes (e.g., bleeding, bruising, swelling, shifting of the brain) which will require immediate treatment (e.g., drugs, surgery). Another diagnostic test used frequently is the MRI (Magnetic Resonance Imaging), which uses a large magnet and a computer to develop pictures of the brain without exposing the patient to x-ray radiation. MRI is believed to give better resolution to brain structures than a CT scan.

Patient course of improvement is also documented via scales such as the Rancho Los Amigos Level of Cognitive Functioning Scale, the Disability Rating Scale, the Functional Independence Measure, and the Functional Assessment Measure. (RK)

Are There Visual Affects Of TBI And What Are They?

TBI is often associated with visuoperceptual problems, particularly when there is gross structural damage sustained on the right side of the brain. Visuoperception is the ability of the brain to understand what it is seeing. Thus, while the optic nerve may be delivering the visual information to the brain normally (visual sensation), the brain is unable to put this information together to determine what it is (perception). Patients with these problems may have difficulty in such areas as reading and recognizing faces or common objects (e.g., one of my patients thought a file cabinet was a set of golf clubs). In extreme situations, patients may become confused, paranoid, and may describe situations, which sound like visual hallucinations. Naturally this problem can be very distressing for the patient and he/she may come to believe that he/she is "going crazy". Education tends to be very effective here, although patients with severe memory deficits may not be able to benefit and may also require medications to decrease their anxiety.

Another common visual problem following a brain injury is visual inattention or neglect. With this deficit, which tends to be particularly associated with parietal lobe lesions in the right hemisphere of the brain, the patient does not pay attention to or completely ignores parts of the body and/or external stimuli on the side opposite the side of the brain that was injured. However, when the patient is consciously made aware of the problem through verbal cues ("look to the left") or visual cues (e.g., a bright color), he/she is able to see the object.

Occasionally, a brain injured patient will have hemianopsia, a visual field cut leading to blindness to a portion or all of the right or left half of vision. In this case, the patient should be encouraged to learn to move his/her head or if possible, the external stimulus itself (e.g., book), until he/she can see it. (RK)

At the time of discharge the charge nurse will discuss with the patient and family the medication the patient is taking, reason for medication possible side effects and how to administer them During the stay on the unit certain patients are given a list of their medications and are encouraged to keep track and ask for them on their own. This familiarizes patients with his medication and how and when to take them Prescriptions will be given to the family to take to their own pharmacy. (NB)

Private insurance company's generally have prescription plans, and Medicaid will also cover for prescriptions, however if you have Medicare (not managed we Medicare) or are Medicaid pending, medication will not be covered and must be purchased by patient/family. (NB)

If the patient is returning home on PEG feedings the nursing staff will meet with patient and family to educate them on this. Teaching the family familiarizes them with the equipment and what to expect when they return home, Social Worker will order all equipment necessary for the PEG feedings including the food. This should be delivered to the home and so up before the patient return home, Upon delivery the worker for the Equipment Company will review how the equipment works. (NB)

The Therapists will recommend equipment to the Physician, the Physician will sip the orders and can also make recommendations, then the Social Worker places the order to the equipment company.

All equipment will be delivered to the Hospital the morning of discharge or may be delivered to the patients home that same day.

It is important to note that not all equipment is coverage each private insurance company (including Medicare) have thew own guidelines. The social worker will check with your insurance company to find out what is a covered item and what will be a private pay item for the family. If it patient has Medicaid, usually all equipment is covered unless it is a specialized item which would need approval from Medicaid.

In some facilities, a self care day is provided. During the self care day the treatment team meet with patient and the family to discuss the patients needs and recommend equipment that will assist the patient in being more functional and independent in the home setting. (NB)

These lands of adjustments as should be discussed with the treatment team as early as possible incase major adjustments need to be made. Project Open House is a program administered by the Mayors office for people with disabilities. This program works to remove architectural barriers in the home of people with mobility impairments and who meet income guidelines. You can check with the Social Worker to we if you are eligible and to file an application. (NB)

The MD and the treatment team will recommend whatever homecare services you will need. Home 'me can include a number of professionals to come into your home to assist with your we and to provide farther rehabilitation, Services could include a RN, home health aide, physical therapist, occupational therapist, speech therapist and social worker. All services must be authorized and approved by your insurance company before services begin. (NB)

What kind of transportation is available to get patients to appointments?

Unfortunately in general private insurance" s including Medicare do not cover for ambulette transportation to therapy or medical appointments, however there am exceptions so you would need to check with your insurance company.

For Medicaid patient's transportation is covered however patient must have an active Medicaid number, Patient must also meet medical criteria for transportation under Medicaid, Medicaid pending will not cover for transportation

For those who qualify there is Access-A-Ride, an application must be filled out but unfortunately the process can take several months for service to be approved, Access-A-Ride charges a small fee for transportation. (NB)