PTP&M004 PTM of Central Nervous System trauma and disease Medical Journal

PHYSICAL THERAPY PRINCIPALS & METHODS PTP&M:0004 Revision: 01 Page: 1 of 56

MANAGEMENT OF CENTRAL NERVOUS SYSTEM

TRAUMA AND DISEASE

NOTICE: This specification, and the subject matter disclosed therein, embody proprietary information which is the confidential property of Mullsons Health & Wellness, which shall be copied, reproduced, disclosed to others, published, and could be used in whole or part, for any purpose, without the express advance written permission of a duly authorized agent of the Company. This specification is subject to recall by Mullsons Health & Wellness at any time.

Medicine: It’s a noble profession, it serves humanity. 1

MANAGEMENT OF CENTRAL NERVOUS SYSTEM TRAUMA AND DISEASE SPEC. BY: Abdulrehman S. Mulla DATE: 03/21/2009 REVISION HISTORY REV.

DESCRIPTION

CN No.

BY

DATE

01 Initial Release PT0001 ASM 03/24/2009



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TABLE OF CONTENTS PAGE 1.0 NERVOUS SYSTEM DISEASES: ............................................................................................................................................................. 3

1.1 THE CENTRAL NERVOUS SYSTEM:...................................................................................................................................... 3 1.1.1 BRAIN: ...................................................................................................................................................................... 4 1.1.2 THE SPINAL CORD:................................................................................................................................................. 7

2.0 SPINAL CORD TRAUMA: ....................................................................................................................................................................... 11 2.1 DEFINITION: ........................................................................................................................................................................... 11 2.2 CAUSES:................................................................................................................................................................................. 11 2.2 SYMPTOMS:........................................................................................................................................................................... 13 2.3 CERVICAL (NEAR THE NECK) INJURIES: ........................................................................................................................... 14 2.4 THORACIC (CHEST-LEVEL) INJURIES: ............................................................................................................................... 15

2.5 LUMBAR SACRAL SHOWN IN PICT:17 (LOWER-BACK) INJURIES ................................................................... 16 2.6 PHYSICAL THERAPY FOR SPINAL CORD INJURY:............................................................................................................ 19

2.6.1 RESPIRATORY CARE: .......................................................................................................................................... 19 2.7 RANGE OF MOTION: ............................................................................................................................................................. 21

2.7.1 INCREASED STRENGTH: ..................................................................................................................................... 22 2,8 MUSCLE STRENGTHENING: ................................................................................................................................................ 22 2.9 COORDINATION AND BALANCE EXERCISES: ................................................................................................................... 23

2.9.1 AMBULATION EXERCISES: .................................................................................................................................. 24 2.9.2 GENERAL CONDITIONING EXERCISES:............................................................................................................. 25 2.11 TRANSFERS: ......................................................................................................................................................... 27

3.0 HEAD INJURY:........................................................................................................................................................................................ 29 3.1 PATHOPHYSIOLOGY: ........................................................................................................................................... 30 3.1.1 HEAD INJURY: ....................................................................................................................................................... 30 3.1.2 BRAIN INJURIES:................................................................................................................................................... 31

3.2 INTRACRANIAL PRESSURE (ICP):....................................................................................................................................... 33 3.2.2 PROGRESSIVE LEVELS OF INTRACRANIAL PRESSURE: ................................................................................ 35 3.2.3 ANOXIC BRAIN INJURY: ....................................................................................................................................... 38

4.0. SPECIFIC TYPES OF HEAD INJURY: ................................................................................................................................................... 39 4.1 SCALP WOUNDS: .................................................................................................................................................................. 39 4.2 SKULL INJURIES:................................................................................................................................................................... 40

4.2.1 SIGNS/SYMPTOMS OF SKULL INJURIES:........................................................................................................... 40 4.2.2 TREATMENT FOR SKULL FRACTURE:................................................................................................................ 41

5-0 GENERAL ASSESSMENT OF HEAD TRAUMA:.................................................................................................................................... 43 5.1 RESPIRATION: ...................................................................................................................................................................... 43 5.2 BLOOD PRESSURE: .............................................................................................................................................................. 44

5.3 PULSE: .................................................................................................................................................................. 44 5.4 GENERAL EXAMINATION: .................................................................................................................................................... 44 5.5 SPECIAL CONSIDERATIONS. BE AWARE THAT: ............................................................................................................... 45 5.6 NEUROLOGICAL EXAMINATION: ......................................................................................................................................... 45

6.0 JUDGING LEVEL OF SEVERITY OF HEAD INJURY: ........................................................................................................................... 46 7.0 LEVELS OF HEAD INJURY: .................................................................................................................................................................. 46

7.1 THE GLASGOW COMA SCALE: ............................................................................................................................................ 46 7.3 POINTS ASSIGNED RESPONSES ON THE GLASGOW COMA SCALE: ........................................................................... 47

7.3.1 EYE OPENING: ...................................................................................................................................................... 47 7.3.2 VERBAL RESPONSE: ............................................................................................................................................ 47 7.3.3 MOTOR RESPONSE:............................................................................................................................................. 47 7.3.4 MEANING OF TOTAL POINTS ON GLASGOW COMA SCALE:........................................................................... 48

8.0 GENERAL MANAGEMENT OF HEAD TRAUMA: .................................................................................................................................. 49 8.1 PHYSICAL THERAPY:............................................................................................................................................................ 49 8.2 PARKINSON'S SPECIFIC PROGRAMMING: ........................................................................................................................ 49 8.3 PHYSICAL THERAPY FOR PARKINSON'S ADDRESSES: .................................................................................................. 50 8.4 PHYSICAL THERAPY FOR INDIVIDUALS WITH PARKINSON’S DISEASE: ....................................................................... 50

8.4.2 CURRENT APPROACHES TO EXERCISE IN PD:................................................................................................ 52 8.5 VESTIBULAR THERAPY: ....................................................................................................................................................... 54

9.0 PREVENTION STRATEGIES: ................................................................................................................................................................ 56



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1.0 NERVOUS SYSTEM DISEASES:

Diseases of the central and peripheral nervous system. This includes disorders of the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction, and muscle.

1.1 THE CENTRAL NERVOUS SYSTEM:

Pict:1



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The Central Nervous System (CNS) is exactly what the name implies. It is the "absolute" central - nervous - system. All of the other nerves that feed off the central - nervous - system are peripheral nerves. These peripheral nerves are part of the peripheral nervous system (PNS). For the purpose of this site, I have separated the Central Nervous System from the Peripheral Nervous System. The Central Nervous System is composed of the Brain and Spinal cord, along with their nerves and end organs (the end of nerves) that control voluntary and involuntary acts. In other words, those physical body processes that you do on your own (moving your arm) and those you do without having to tell your body to do it (like breathing). The parts of the brain governing consciousness and mental activities are; parts of the brain, spinal cord, and their sensory and motor nerve fibres controlling skeletal muscles; and end organs of the body wall. Your CNS is the Master Control Centre, the CEO, the Commander in Chief, the Big Kuhuna, The Master Communicator and the Grand Pooh-Bah all rolled into one!

1.1.1 BRAIN: The brain is a large soft mass of nerve tissue that is contained inside a vault of bone called the cranium. It is the cranial portion of the CNS. The brain is also called the "encephalon." The brain is composed of neurons (nerve cells) and neuralgia (supporting nerve cells). The brain consists of gray and white matter. The gray matter is nervous tissues of a grayish color that forms an "H" shaped structure and is surrounded by white matter.

Pict:2

The human brain has more than 10 billion nerve cells and over 50 billion other cells and now weighs on an average of 3 1/8 pounds, where it used to weigh less than 3 pounds. The brain monitors and regulates your unconscious bodily functions like breathing and heart rate, and coordinates most of your voluntary movement. It is also the area of consciousness, thought and creativity!



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Different areas of your brain perform different functions: Receive messages from sense organs Interpreting images from the eye Controls balance and muscle coordination Thoughts and creativity In charge of speech and reading Basis of perception In charge of feeling emotion Initiates activity in the glands and muscles Basic motor skills Is the seat of consciousness, memory, reason and judgment Figuring complex calculations Regulates circulation and respiration

Pict:3

The central nervous system, gives rise to the peripheral nervous system as shown in Pict:4 (the nerves on the periphery of the body). The autonomic nervous system (ANS) is under control of central nervous system and is also part of the peripheral nervous system, although these nerves stay within the body and effect organs and soft tissues and do not leave to effect appendages (arms and legs). The autonomic nervous system (ANS) is "automatic" and in control of involuntary bodily functions and it is divided into two parts: The sympathetic and parasympathetic nervous system. It regulates the function of glands, the adrenal medulla, smooth muscle tissue, organs and the heart.



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Pict:4 Pict:5



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1.1.2 THE SPINAL CORD:

The spinal cord is an ovoid column of nervous tissue that averages about 44 cm in length when it is flattened out. The spinal cord extends from the medulla oblongata in the brain stem to the 2nd lumbar vertebra in the spinal canal. All of the nerves in your arms, legs and trunk originate from the spinal cord. The spinal cord is the center of reflexive action. When you are stimulated in any way, shape or form, there is a reflex arc that goes from the peripheral nerve to the spinal cord, up to the brain and back down to relay the action. That's some pretty quick service from your CNS as shown in Pict:6. Especially when you just about drop something and catch it quickly or if you are Andy Roddick hitting a150 mph tennis ball at the 2004 Davis Cup.

Pict:6



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Pict:6

The spinal cord is housed in a vertebral (bony) vault for its own protection. The spinal cord travels down through a hole in each vertebrae. If you were to see the spinal cord in a cross-section, you would notice that it does not fill the vertebral space in the vertebral column, it is surrounded by other tissue (pia mater as shown in Pict:9), cerebrospinal fluid (CSF as shown in Pict:8), another tissue (arachnoid mater as shown in Pict:9), and still another tissue (dura mater as shown in Pict:9). The three types of mater are called the meninges. The meninges also surround the brain. Hence the word "meningitis" when there is an inflammation of the meninges or membranes of the spinal cord or brain.

Pict:8



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Pict:9

Cerebrospinal fluid (CSF) when normal contains 50 - 75 mg of sugar per 100 ml. The sugar content is lower than that of blood. The CSF is a water cushion protecting the brain and spinal cord from physical impact.



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The "H" shape from the gray matter inside the white matter in the brain is carried through the spinal cord as well because they are attached to one another. The anterior "horn" of the "H" is composed of motor cells from the fibers that make up the motor portions of the peripheral nerves as shown in Pict:10. The sensory neurons as shown in Pict:11 enter the posterior "horn" of the "H." Incidentally, the "H" does not mean "horn" although the "H" formation does represent the anterior and posterior sides at which the nerves enter.

Pict:10

Sensory Neurons carry impulses away from the spinal cord and brain to muscles or glands

Pict:11



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2.0 SPINAL CORD TRAUMA:

2.1 DEFINITION:

Spinal cord trauma (Spinal cord injury; Compression of spinal cord) is damage to the spinal cord. It may result from direct injury to the cord itself or indirectly from damage to surrounding bones, tissues, or blood vessels.

2.2 CAUSES: Spinal cord trauma can be caused by any number of injuries to the spine. They can result from motor vehicle accidents, falls, sports injuries (particularly diving into shallow water), industrial accidents, gunshot wounds, assault, and other causes. A minor injury can cause spinal cord trauma if the spine is weakened (such as from rheumatoid arthritis or osteoporosis) or if the spinal canal shown in Pict:12 protecting the spinal cord has become too narrow (spinal stenosis shown in Pict:13) due to the normal aging process.

Pict:13



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Direct injury, such as cuts, can occur to the spinal cord, particularly if the bones or the disks have been damaged. Fragments of bone (for example, from broken vertebrae, which are the spine bones) or fragments of metal (such as from a traffic accident) can cut or damage the spinal cord.

Direct damage can also occur if the spinal cord is pulled, pressed sideways, or compressed. This may occur if the head, neck, or back are twisted abnormally during an accident or injury.

Bleeding, fluid accumulation, and swelling can occur inside the spinal cord or outside the spinal cord (but within the spinal canal). The accumulation of blood or fluid can compress the spinal cord and damage it.

Most spinal cord trauma happens to young, healthy individuals. Men ages 15-35 are most commonly affected. The death rate tends to be higher in young children with spinal injuries.

Risk factors include participating in risky physical activities, not wearing protective gear during work or play, or diving into shallow water.

Older people with weakened spines (from osteoporosis) may be more likely to have a spinal cord injury. Patients who have other medical problems that make them prone to falling from weakness or clumsiness (from stroke, for example) may also be more susceptible.



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2.2 SYMPTOMS:

Symptoms vary somewhat depending on the location of the injury. Spinal cord injury causes weakness and sensory loss at and below the point of the injury. The severity of symptoms depends on whether the entire cord is severely injured (complete) or only partially injured (incomplete). The spinal cord doesn't go below the 1st lumbar vertebra, so injuries at and below this level do not cause spinal cord injury. However, they may cause "cauda equina syndrome" injury to the nerve roots in this area, shown in Pict:14.

Pict:14



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2.3 CERVICAL (NEAR THE NECK) INJURIES:

When spinal cord injuries occur near the neck shown in Pict:15, symptoms can affect both the arms and the legs:

Breathing difficulties (from paralysis of the breathing muscles) Loss of normal bowel and bladder control (may include constipation, incontinence,

bladder spasms) Numbness Sensory changes Spasticity (increased muscle tone) Pain Weakness, paralysis

Pict:15



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2.4 THORACIC (CHEST-LEVEL) INJURIES: When spinal injuries occur at chest level, symptoms can affect the legs: Breathing difficulties (from paralysis of the breathing muscles) Loss of normal bowel and bladder control shown in Pict:16 (may include constipation, incontinence, bladder spasms) Numbness Sensory changes Spasticity (increased muscle tone) Pain Weakness, paralysis Injuries to the cervical or high-thoracic spinal cord may also result in blood pressure problems, abnormal sweating, and trouble maintaining normal body temperature.

Pict:16



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2.5 LUMBAR SACRAL SHOWN IN PICT:17 (LOWER-BACK) INJURIES

When spinal injuries occur at the lower-back level, varying dgrees of symptoms can affect the legs:

PICT:17

Loss of normal bowel and bladder control (may include constipation, incontinence,

bladder spasms) Numbness Pain Sensory changes Spasticity (increased muscle tone) Weakness and paralysis

The following tests may be ordered:

A CT scan or MRI of the spine may show the location and extent of the damage and reveal problems such as blood clots (hematomas shown in Pict:18).

Myelogram (an x-ray of the spine after injection of dye shown in Pict:19) may be necessary in rare cases.

Somatosensory shown in Pict:20 evoked potential (SSEP) testing or magnetic stimulation may show if nerve signals can pass through the spinal cord.

Spine x-rays shown in Pict:21 may show fracture or damage to the bones of the spine.



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Pict:18

Pict:19



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Pict:20

Pict:21



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2.6 PHYSICAL THERAPY FOR SPINAL CORD INJURY: Physical therapists are involved in many aspects of patient care following a spinal cord injury. The major areas are as follows:

Respiratory Care Range of Motion Muscle Strengthening Balance Wheelchair Skills Transfers Skin Care

2.6.1 RESPIRATORY CARE: When in the intensive care unit, physical therapists can help teach you how best to breath and cough using many hands-on techniques. They will also suction the mucous out of your lungs if necessary. A physical therapist's purpose with respiratory care is to help you breathe easier and to decrease your chance of developing a lung infection such as pneumonia. Respiratory complications of spinal cord injury (SCI), including:

Atelectasis Pneumonia Respiratory failure Pulmonary embolism Pleural effusion Sleep-disordered breathing

2.6.1.1 MANAGEMENT:

1. Prevention and treatment of atelectasis and pneumonia. Monitoring indicators Intubation (for intractable respiratory failure, demonstrable

aspiration, or high risk for aspiration plus respiratory compromise) Specific tests of pulmonary mechanics and ventilation Clearing the airway of secretions Diaphragm fluoroscopy Reexpansion of the affected lung tissue following successful

treatment (required for atelectasis or pneumonia)



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2. Mechanical ventilation.

Recognizing role of surfactant production Positive-end expiratory pressure (PEEP) Monitoring for pulmonary embolism and pulmonary effusion Treatment of complications of short and long-term ventilation Evaluation of the need for long-term ventilation

3. Weaning from the ventilator.

Progressive ventilator-free breathing (PVFB) Synchronized intermittent mandatory ventilation (SIMV) Partial weaning

4. Evaluation for electrophrenic respiration 5. Polysomnographic evaluation 6. Positive airway pressure therapy (if sleep disordered breathing is

diagnosed) 7. Evaluation for and prevention of dysphagia and aspiration 8. Tracheostomy (for patients who are aspirating) 9. Psychosocial assessment and treatment

Monitoring of patient's post-injury feeling states Assessment of substance abuse Assessment of pain Establishment of advance directives Assistance and support of family caregivers Addressing of intimacy and sexuality issues (with the patient and

other appropriate parties) Establishment of an effective communication system.

2.6.1.2 DISCHARGE AND FOLLOW-UP: 1. Education of patient and caregivers 2. Evaluation and modification of patient's home 3. Provision of appropriate medical equipment and personnel resources 4. Transportation assistance 5. Evaluation of financial resources and available benefits 6. Determining the availability of transition and leisure resources 7. Vocational evaluation



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2.7 RANGE OF MOTION:

Physical therapists help to maintain or increase your joint range by stretching your muscles and moving your joints. It is important to keep your joints mobile in order to increase your ability to move and perform everyday functions. Range of motion can also help to decrease you pain.

Range of motion in joints is often impaired after injury, illness, or surgery. When range of motion is lost, your physical therapist may use joint and soft tissue mobilization or stretching exercises to restore more useful, full movement. See Pict:22 .

Joint and soft tissue mobilization is a unique, hands-on technique that allows the physical

therapist to release restrictions around joints and throughout the soft tissue system. By releasing these restrictions your physical therapist works to achieve your full potential range of motion in an area of dysfunction.

Stretching exercises help to restore length to soft tissue that has shortened and lost

elasticity. Your physical therapist may help you stretch specific areas and then teach you a stretching program to continue at home. Physical therapists also teach stretching to help prevent back problems and athletic injuries.

Pict:22



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2.7.1 INCREASED STRENGTH:

Movement depends on adequate muscle strength. Muscles may weaken from surgery, injury, or simply from not being used. Physical therapists can help improve strength by making muscles work harder through exercise and electrical stimulation.

Exercise has benefits beyond increasing strength. An exercise program designed by your physical therapist also improves coordination, endurance, and circulation. Your physical therapist will develop a program to meet your abilities, lifestyle, age, and specific goals for therapy.

Electrical stimulation may be used when muscles are immobilized (such as when

a limb is casted after surgery) or when muscles are extremely weak. To exercise these muscles, an electrical impulse is sent through the skin causing muscles to contract automatically

2,8 MUSCLE STRENGTHENING:

Following a spinal cord injury, it is very important for you to increase your strength in all muscles that you still have control over. These muscles will have to work much harder than they did before the injury in order to compensate for lost movements. Physical therapists can teach you the correct exercises to increase the strength of specific muscles without causing injuries. Many forms of exercise increase muscle strength. All involve progressively increased resistance. When a muscle is very weak, movement against gravity alone is sufficient. As muscle strength increases, resistance is gradually increased by using stretchy bands or weights. In this way, muscle size (mass) and strength are increased, and endurance improves.

Pict:23



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2.9 COORDINATION AND BALANCE EXERCISES:

These exercises can help people who have problems with coordination and balance, usually because of a stroke or brain damage. Coordination exercises aim to help people do specific tasks. The exercises involve repeating a meaningful movement that works more than one joint and muscle, such as picking up an object or touching a body part. Balance exercises are initially done using parallel bars, with a therapist standing right behind the person. The person shifts weight between the right and left legs in a swaying motion. Once this exercise can be done safely, weight can be shifted forward and backward. When these exercises are mastered, the person can do them without parallel bars.

Pict:24



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2.9.1 AMBULATION EXERCISES: Walking (ambulation)—independently or with assistance—may be the main goal of rehabilitation. Before starting ambulation exercises, people must be able to balance while standing. To improve balance, people usually hold onto parallel bars and shift weight from side to side and from front to back. To keep them safe, the therapist stands in front of or behind them. Some people need to improve a joint's range of motion or muscle strength. Some people need an orthotic device such as a brace. See Pict:23

Pict:23

When people are ready for ambulation exercises, they may begin on parallel bars, then progress to walking with mechanical aids, such as a walker, crutches, or a cane. Some people need to wear an assistive belt, which the therapist uses to prevent them from falling. As soon as people can walk safely on a level surface, they may be taught how to step over curbs or to climb stairs. When climbing up stairs, they are instructed to step up with the unaffected leg first. To climb down stairs, they are instructed to step down with the affected leg first. The phrase "good is up, bad is down" can help people remember. Family members and caregivers who help people walk should learn how to support them correctly.



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2.9.2 GENERAL CONDITIONING EXERCISES:

A combination of range-of-motion, muscle-strengthening, and ambulation exercises is used to counter the effects of prolonged bed rest or immobilization. General conditioning exercises help improve cardiovascular fitness (the ability of the heart, lungs, and blood vessels to deliver oxygen to working muscles), as well as maintain flexibility and muscle strength.

Pict: 24



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2.10 WHEELCHAIR SKILLS:

A large amount of people who have had a spinal cord injury will have to use a wheelchair at least some of the time. Using a wheelchair allows you to get where you want to go as independently as possible. In order to independently move your wheelchair, there are many skills that you have to learn. These vary from simple skills such as maneuvering wheelchair safety to more complex skills such as climbing curbs and ramps.

Pict: 25



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2.11 TRANSFERS: Depending on where your injury is, most spinal cord injured patients can learn to get in and out of their bed and wheelchair independently. Physical therapists help teach you the easiest way for you to transfer and move around. For many people (particularly those who have had a hip fracture, an amputation, or a stroke), transfer training is a critical goal of rehabilitation. Being able to transfer safely and independently from bed to chair, chair to toilet, or chair to a standing position is essential to remaining at home. People who cannot transfer without help usually require 24-hour assistance. Caregivers may help them transfer using special devices, such as a gait belt or harness. See: Pict 26

Pict 26 The techniques used in transfer training depend on the following:

Whether people can bear weight on one or both legs Whether they can balance well Whether they are paralyzed on one side of the body

Assistive devices can sometimes help. For example, people who have difficulty standing from a seated position may benefit from a seat-lifting chair or a chair with a raised seat. See: Pict 27

Pict 27

Tilt Table: see Pict 28 If people have been limited to strict bed rest for several weeks or have had a spinal cord injury, they may get dizzy when they stand up (orthostatic hypotension—see Low Blood Pressure: Orthostatic Hypotension). A tilt table may be used to help such people. This procedure may retrain blood vessels to narrow (constrict) and widen (dilate) appropriately in



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response to changes in posture. People lie face up on a padded table with a footboard and are held in place with a safety belt. The table is tilted very slowly, determined by how well people tolerate it, until they are nearly upright. The slow change in posture enables the blood vessels to regain the ability to constrict. How long the upright position is maintained depends on how well people tolerate it, but it should not exceed 45 minutes. The tilt-table procedure is done once or twice a day. Its effectiveness varies depending on the type and degree of disability.

Pict 28



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3.0 HEAD INJURY:

Few nonfatal injuries cause such devastating physical and psychological effects as trauma to the central nervous system. In many cases, irreversible damage occurs regardless of the care the victim receives. In a significant number of cases, however, the initial care administered determines the ultimate outcome of the case. In fact, in such "treatable" patients, the emergency management is frequently more important than all subsequent efforts. This statement should trigger in your mind the importance of your role in the evaluation and initial care of these patients. a. The most important initial indicator of the severity of a head injury is the patient's level of

consciousness. A competent observer should assess the patient's consciousness level as soon as possible after the injury has occurred. A severe head injury may be defined as one that leaves the patient unconscious for at least 6 hours. A patient who has an altered level of consciousness less severe and for a shorter time period may have medical problems much later, problems caused by the injury.) Therefore, a patient with any level of impaired consciousness after a head injury should be treated as though he has a serious head injury. See Pict 29.

b. The majority of head injuries are mild and self-limiting. However, since severe head injuries can be

life-threatening, it is important to assess and treat a head injury correctly to prevent death or disability from secondary brain damage.

Pict: 29



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3.1 PATHOPHYSIOLOGY: Pathophysiology is the physiology of disordered function. When there is trauma to the central nervous system in the form of a head injury, a variety of pathophysiological responses can occur.

3.1.1 HEAD INJURY: See: Pict:30 The words "head injury" usually refer to an injury to the portion of the skull (cranium) that encloses the brain, the overlying scalp, or the contents of the cranial cavity (brain, cranial nerves, meninges, and associated blood vessels). This definition focuses attention on that portion of the head that is at or above the level of the eyebrows anteriorly, the zygomatic arches laterally, and an imaginary line between the tips of the mastoid processes posteriorly. These are approximate external landmarks for the skull base, which is the floor of the cranial cavity. Nevertheless, physical signs of injury of the brain or of its soft tissue or bony coverings may also be detected in adjacent structures of the head (eyes, ears, and nose) or even in portions of the body that are remote from it.

Pict:30



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3.1.2 BRAIN INJURIES: Most brain injuries occur due to movement of the brain inside the skull. The level of damage to the brain depends on the speed the head was traveling and the head's position just prior to contact.

Pict:30

3.1.3 RESPONSES TO BRAIN INJURY:.

The base of the skull is rough; therefore, movement over this area will cause various degrees of injury to the brain or blood vessels. Possible responses to brain injury include the following: a. Initial response to a bruised brain is swelling. The swelling is caused by:

Increased blood volume due to vasodilation and increased cerebral blood flow to the injured areas.

Buildup of extra blood volume putting pressure on the brain and decreasing blood flow to the injured part.

NOTE: Since the edema builds over a period of 24 to 48 hours, early care and efforts

to decrease the vasodilation is important. b. Carbon dioxide may build up, having a critical effect on cerebral vessels. This

buildup causes more vasodilation. c. Hyperventilation may occur, causing a decrease in the carbon dioxide,

vasoconstriction, and better perfusion (passage of a fluid through the vessels of an organ) for the brain.



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NOTE: Hyperventilation -- a condition marked by fast, deep breathing, which tends to remove increased amounts of carbon dioxide from the body and lower the partial pressure of the gas, causing buzzing in the ears, and tingling of the lips and fingers. See picture 31

Pict. 31 d. Unconsciousness may occur due to injury to the cerebral cortex or the brain stem. See picture 32.

Pict. 32. e. If there is increased intracranial pressure (ICP) and decreasing cerebral blood flow, no matter what

the cause, the level of consciousness is depressed. f. The intracranial cavity is filled to capacity with contents that cannot be compressed

-- cerebral spinal fluid, intravascular blood, brain tissue water (interstitial fluid). If the volume of one of the constituents of the intracranial cavity increases, a



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reciprocal decrease in volume of one or both of the others must occur. Otherwise, the result is an increase in intracranial pressure.

3.2 INTRACRANIAL PRESSURE (ICP):

Pict:33

NOTE: Intracranial pressure monitoring is performed by inserting a catheter

into the head with a sensing device to monitor the pressure around the brain. An increase in intracranial pressure can cause a decrease in blood flow to the brain causing brain damage.



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3.2.1 CHANGES CAUSED BY INTRACRANIAL PRESSURE:

A patient with head injury may experience an alteration in his level of consciousness. Other symptoms associated with a severe head injury may include convulsions, delirium, coma, paralysis, and increased intracranial pressure, which will be discussed here. The skull (a container that cannot expand) holds the brain, vascular tissue, and cerebrospinal fluid. Any problem (trauma, edema, tumor, infection, or bleeding) which adds to the contents of the skull will result in an increase in intracranial pressure in the skull. That increased pressure sets off the changes listed below:

a. As the intracranial pressure increases, the blood vessels are squeezed from the

outside, restricting blood flow throughout the arteries. b. As the brain notes a drop in blood pressure, the sympathetic defenses respond,

causing the blood pressure to increase. c. Respiratory changes occur due to the chemoreceptors that sense changes in the

blood chemistry. d. The vagus nerve is affected, causing the pulse to slow. e. Cushing's response - Increased blood pressure characterized by slow pulse. This

is a clear but late sign of increased intracranial pressure. f. As the intracranial pressure progresses, the level of consciousness is altered.

Eventually, unconsciousness occurs because the body's vital functions cannot operate properly. Ultimately, there is brain death due to loss of adequate cerebral perfusion (passage of fluid through the brain).

g. Once the brain's ability to compensate is exhausted, the areas of the brain shift, causing herniation.

NOTE: Compression may be from above (central syndrome) or from the side (lateral syndrome). The central syndrome progresses in a more orderly manner and causes unconsciousness early.



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3.2.2 PROGRESSIVE LEVELS OF INTRACRANIAL PRESSURE: Three progressive levels of intracranial pressure can be identified.

1. Progressive level one.

a. Involves cerebral cortex and upper brain stem. b. Blood pressure rises, pulse slows. c. Pupils appear small but are reactive. d. Abnormal respiratory pattern noted (possibly Cheyne-Stokes). e. Initially, patient will try to remove painful stimuli. Later, the patient withdraws from

pain. f. As progression occurs, the pain will cause decorticate posturing (flexion of the

upper extremities with lower extremities becoming rigid and extended). g. Still reversible.

Pict:34



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2. Progressive level two.

a. Middle portion of the brain stem is involved. b. Blood pressure increases. c. Pulse slows. d. Pupils become fixed at 3 to 5 mm and nonreactive or only sluggishly reactive

to light. e. Abnormal respiratory pattern: fast, shallow panting (neurogenic

hyperventilation).

Pict:35



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3. Progressive level three.

a. Pupils become fixed and dilated. b. If only one "blown" pupil, it will be on the same side as the hematoma or

swelling. (Crossover of nerves occurs at about the lip level.) c. Document which pupil dilates first. d. Respiratory ataxia (erratic, no rhythm) or absent. No response to painful

stimuli. e. Pulse is rapid and irregular. f. Decreased blood pressure.

Pict:36



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3.2.3 ANOXIC BRAIN INJURY: Anoxic brain injury is injury to the brain from lack of oxygen (from cardiac arrest, choking, or drowning). Spasms develop in small arteries if the brain goes without oxygen for more than 4 to 6 minutes. Blood flow does not reach the cerebral cortex. The level of brain damage is based on the length of anoxia (lack of oxygen). See pict.37

Pict.37



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4.0. SPECIFIC TYPES OF HEAD INJURY:

4.1 SCALP WOUNDS:

The scalp has many blood vessels, a number of which are close to the surface. A scalp laceration, therefore, may bleed profusely even though a major blood vessel has not been cut. Initially, even a minor laceration may bleed a great deal. Normally, blood in the scalp clots rapidly, and blood flow can be controlled easily. If necessary, bleeding can usually be controlled by direct pressure; that is, by compressing the scalp between the fingertips and the skull. It is important to control bleeding in both adults and children, but it is especially important in children because they have a smaller volume of blood. See picture 38.

Pict: 38



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4.2 SKULL INJURIES: The skull is composed of the cranium and the face. Skull fractures are commonly fractures to the cranium rather than the face.

Pict:39

4.2.1 SIGNS/SYMPTOMS OF SKULL INJURIES: The most obvious signs of a skull fracture are visible bone fragments and bits of brain tissue. The possibility of a skull fracture exists when any of the following less obvious signs/symptoms are present: a. Following an injury, the patient may be either unconscious or have an altered level

of consciousness. b. The patient has sustained an injury that has caused a deep laceration or severe

bruises to the scalp or forehead. c. There is severe pain or swelling at the site of a patient's head injury. d. There is a deformity of the patient's skull; for example, a depression in the

cranium, a large swelling, or anything that looks unusual about the cranium's shape.

e. The patient has a bruise or swelling behind the ear (Battle's sign - discoloration behind the ear caused by a fracture in the base of the skull). This sign may appear hours to days after the injury.

f. The pupils of the patient's eyes are unequal in size.



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g. Tissue around or under both eyes of the patient are discolored ("black eye(s)" or "raccoon eyes"). This discoloration may appear hours after the injury.

4.2.2 TREATMENT FOR SKULL FRACTURE:

4.2.2.1 FOLLOW THESE GENERAL PROCEDURES:

1. Assure/maintain an open airway. 2. Resuscitate, if necessary. 3. Keep the patient at rest; do not let him move around. 4. Control bleeding. 5. Monitor the patient's vital signs. 6. Dress and bandage any open wounds. 7. Try to keep a conscious patient alert by talking to him. Ask him

questions to force him to concentrate. 4.2.2.2 REMEMBER:

1. DO NOT put pressure on an obvious skull fracture. 2. DO NOT try to remove penetrating objects. Leave them in place and

transport the patient. 4.2.2.3 If the patient has no hematoma, infection, or cerebral spinal fluid leak,

a skull fracture presents no danger at this time. 4.2.2.4 CONCUSSION:

A concussion is a mild state of stupor or temporary unconsciousness caused by a blow to the head. In this condition, there is no laceration or bleeding in the brain. There is no significant injury to the brain itself. 1. Signs/symptoms of concussion. Signs and symptoms of a concussion

occur immediately. Included are the following: a. Knowledge that the patient has received a blow to the head, has had

a temporary loss of consciousness, and memory loss are indications of a concussion.

b. The most important indication of concussion is memory loss for the exact moment of injury. This is a sign of brain dysfunction. The patient may never remember the exact moment of injury. His brain had not had time to record the moment in his memory. Sometimes, the patient cannot remember events just preceding the moment of injury, a condition called retrograde. Or, a patient may not be able to remember events that happened just after the moment of injury, this condition being called antigrade. Short time memory loss may cause a patient to ask questions repeatedly about the moments surrounding his injury.

c. The patient may become combative. d. Not all patients who have a concussion lose consciousness. But

those who do may regain consciousness anywhere from a few



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minutes to an hour. If the loss of consciousness was only momentary, often neither the patient nor witnesses are sure whether or not the patient lost consciousness.

2. Treatment for concussion. There is no specific treatment for a

concussion. If the patient is not being detained for observation, a responsible adult should be told to check on the patient hourly. The adult should be told the signs/symptoms that would indicate that the patient needs further medical help. Usually, within 24 to 48 hours, the symptoms of concussion begin to subside.

4.2.2.5 CEREBRAL CONTUSION:

A focal brain injury is an injury in which there is dysfunction of a particular region, system, or side of the brain. The most common type of focal brain injury is a cerebral contusion. This type of contusion is a bruise in the brain that consists of a superficial focus of brain hemorrhage, necrosis, and/or laceration.

1. Types of cerebral contusions. Included are the following:

a. Coup contusion. This type of contusion occurs in the part of the brain that is directly under the focus of an impact.

b. Contrecoup contusion. This contusion occurs in areas of the brain that are remote from the focus of impact. I. Blows to the back of the head commonly cause this type of

contusion. A contrecoup contusion can, however, be caused by a blow to any part of the head.

II. There is scientific disagreement on exactly how a contrecoup contusion occurs. One theory is that the impact of something on the skull accelerates or decelerates the brain within the cranial cavity. The result is that the brain collides with the inner surface of the skull and becomes bruised.

2. Treatment. Patients with cerebral contusion require hospitalization for observation.

4.2.2.6 INTRACRANIAL HEMATOMA:

Intracranial hematoma (within the cranium, a swelling that contains blood) is a rare injury, but important because this injury is the most common cause of preventable death following a head injury. Two classifications of traumatic intracranial hematomas are acute epidural hematomas and acute subdural hematomas.

1. Acute epidural hematoma. This type of hematoma is an accumulation of

blood between the dura (the thick, dense, fibrous layer which covers and protects the brain and the spinal cord) and the inner surface of the skull. The cause of an acute epidural hematoma is either a tear in a meningeal artery within the dura or an impact injury to a dural venous sinus. Since the bleeding is arterial, pressure builds rapidly and death can occur



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quickly. But, the prognosis for recovery is good if the patient is diagnosed correctly and treated early. Signs and symptoms of acute epidural hematoma include the following: a. A history of head trauma. b. Initial loss of consciousness. c. Next, a period of consciousness and coherence. d. Patient lapses back into unconsciousness. e. Patient develops paralysis on the opposite side of the injury with

dilated/fixed pupils of the eye on the same side as the injury. f. If not treated, paralysis is followed by death.

NOTE: The time when the patient is lucid and relatively alert is the period between the recovery from the primary brain injury (usually a concussion) and the onset of signs/symptoms of brain distortion/displacement by the hematoma. When you know that a person has had a blow to the head and you see this lucid period between periods of unconsciousness, suspect the presence of an acute epidural hematoma.

2. Acute subdural hematoma. An acute subdural hematoma is caused by a

high velocity impact. This type of hematoma comes from venous bleeding located between the dura and the brain. The impact damages the underlying brain tissue. Signs/symptoms include: Headache. Fluctuation in the level of consciousness. Semiparesis (muscular weakness/ mild paralysis on one side of the body).

NOTE: If surgery is performed less than 4 hours after the injury, the recovery rate for a patient with intracranial hematoma is about 90 percent. If surgery is performed more than 4 hours after the injury, the recovery rate is about 30 percent. Even a patient with acute intracranial hematoma has a better chance of recovery with early operative treatment.

GENERAL NOTE: Generally, patients with head trauma injury should be hyperventilated to get as much oxygen to the cells as possible and to lower intracranial pressure (pressure within the skull).

5-0 GENERAL ASSESSMENT OF HEAD TRAUMA:

Approximately 40 percent of serious trauma victims have central nervous system injuries. This group has a death rate twice as high (35 percent versus 17 percent) as that of victims without central nervous system injuries. Estimations are that head injuries account for 25 percent of all trauma deaths and up to one-half of all motor vehicle fatalities. The head-injured victim will rarely be cooperative and is often under the influence of alcohol. When evaluating a patient with a head injury, always assume that the patient also has a spinal cord injury.

5.1 RESPIRATION:

A head injury produces several types of abnormal respiratory patterns. Possible abnormalities include: 1. A slowed respiratory rate caused by an acute rise in intracranial pressure. 2. A rapid respiratory rate can be caused if the intracranial pressure continues to rise.



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3. Respirations may be noisy. 4. Kussmaul and Cheyne-Stokes patterns are often caused by the metabolic causes of coma.

5.2 BLOOD PRESSURE: Over a period of time, note any changes in the patient's blood pressure. The rise or fall of blood

pressure can indicate changes in the patient's condition or further injury. 1. Rising blood pressure. Generally, blood pressure rises if intracranial pressure rises. The

systolic blood pressure in particular will rise. The effect is a widening of pulse pressure (pulse pressure = systolic blood pressure minus diastolic blood pressure). Therefore, if the patient's blood pressure rises without any medical explanation, he may experience a rise in intracranial pressure.

2. Falling blood pressure. If the patient's blood pressure is falling, he may have an injury which has not been discovered and treated. The skull is a very small box which is almost full of brain. Therefore, there is very little room in the skull for blood. If the patient is in hypovolemic shock (shock produced by reduction of blood volume, possible cause is hemorrhage), he is probably bleeding somewhere other than the head. Look for a source of major hemorrhage somewhere else in the body.

5.3 PULSE: A change in pulse rate (either increasing or decreasing) may indicate a serious problem. Note the following conditions: 1. A slowing pulse will usually accompany the rise in blood pressure observed in a patient

with rising intracranial pressure. A continued rise in intracranial pressure can produce tachycardia (abnormally fast heart beat), causing death.

2. A rising pulse rate may signal impending shock from bleeding elsewhere in the body. 3. A rapid pulse without another cause is a serious sign. 4. Bradycardia (an abnormally slow heartbeat) with hypertension suggests a rapidly

expanding hematoma.

5.4 GENERAL EXAMINATION: A general examination should include the following: 1. Check the scalp or skull for lacerations or fractures. 2. Fluid from the ears and nose should be checked for the presence of spinal fluid. Soak up a

small amount of drainage from the ears or nose with a 4 x 4 gauze square. Cerebral spinal fluid will form a ring around the blood.

3. Any trauma above the clavicle (collarbone) should suggest cervical spine injury. 4. Consider that the patient may have cervical spine injury and immobilize his head and neck

if: a. The mechanism of injury suggests violent action to the spine. b. The patient has a severe head injury. c. Injury to the patient resulted in:

I. Loss of consciousness. II. Markedly altered level of consciousness. III. Display of specific signs of neurological deficit (motor or sensory).



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5.5 SPECIAL CONSIDERATIONS. BE AWARE THAT: 1. Drugs and alcohol will frequently change the level of consciousness and cloud significant

signs and symptoms of the trauma patient. 2. Altered respiratory patterns may be caused by other injuries and by uncorrected

hypovolemia (markedly diminished blood volume). 3. Metabolic abnormalities can alter respiratory function. 4. Blood pressure elevation may be caused by pain, anxiety, or preexisting hypertension. 5. Only at the terminal stages of head injury does the patient exhibit hypotension as the result

of head injury itself. 6. Assume a patient with low blood pressure is hemorrhaging elsewhere and treat for shock.

7. Repeat examinations at intervals and record accurately. Look for trends and changes such

as: a. Significant rise in blood pressure. b. Slower pulse occurring late in the cycle.

5.6 NEUROLOGICAL EXAMINATION:

A neurological examination is performed to assess the patient's condition at the time he is being examined. 1. AVPU for initial assessment. The letters AVPU stand for methods of assessing a patient's

responsiveness or unresponsiveness. The patient will be checked for alertness, verbal responsiveness, pain responsiveness, and, finally, unresponsiveness. a. Alertness to stimuli. b. Responds to verbal stimulus. c. Responds to painful stimulus. d. Unresponsive to stimuli.

2. Glasgow coma scale for secondary assessment. Patient responses in these areas are checked: a. Eye opening. b. Verbal response. c. Motor response.

3. Evaluation of pupils for equality/reaction to light. Check the patient's eyes for normal or abnormal reactions as follows: a. Normal reactions include:

I. When exposed to light, the pupils constrict. II. When light is shined into one pupil, the other pupil also constricts.

b. Abnormal reactions include: I. Pupils are fixed and pinpoint. II. Drooping upper eyelid when eyes are open (ptosis). III. One pupil dilated and fixed. IV. Both pupils dilated and fixed.



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6.0 JUDGING LEVEL OF SEVERITY OF HEAD INJURY:

The most important indication of the severity of a patient's head injury is the patient's level of consciousness. His initial level of consciousness is also the best indicator of how well the patient will recover from the head injury. A changed level of consciousness reflects the degree of generalized injury to the brain. Initially, the patient's level of consciousness can be assessed by testing his responses to stimuli using the AVPU test.

6.1 A - Is the patient alert? Is the patient looking around to find out where he is? 6.2 V - Does the patient respond to verbal stimuli? When asked a question, does the patient

respond well or at all? 6.3 P - Does the patient respond to painful stimuli? Does the patient respond to a pinch or a pin

prick? 6.4 U - Is the patient unresponsive? Does the patient respond to no stimuli at

7.0 LEVELS OF HEAD INJURY:

7.1 THE GLASGOW COMA SCALE: The Glasgow Coma Scale (GCS) is the most widely used system of defining the level of consciousness of head-injured patients. Older classification systems relied on descriptive terms such as obtundation (diminished pain or touch sensations), stupor, semicoma, etc. These terms sometimes meant different signs/symptoms to different people. The Glasgow Coma Scale defines the level of consciousness according to three functions: eye-opening, language function (verbal response), and movement (motor response).

7.2 RESPONSES OF GLASGOW COMA SCALE:

Each of these functions has a set of subscales made up of a hierarchy of responses which are assigned numerical values (points). The patient is stimulated, his response is observed, and a point value is given based on the response. The person examining the patient tries to draw out the best response from the patient. The total number of points from these patient responses defines a level of consciousness (recognized worldwide) and indicates the severity of the head injury.



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7.3 POINTS ASSIGNED RESPONSES ON THE GLASGOW COMA SCALE: The points assigned patient responses are as follows:

7.3.1 EYE OPENING: Examiner determines the best eye response in accordance with the following response

grading scale: a. Eyes open spontaneously -- 4 points. b. Eyes open in response to speech -- 3 points. The patient opens his eyes when he

is told to do so, or he responds to a command. c. Eyes open in response to noxious stimuli -- 2 points. d. Eyes do not open in response to noxious stimuli --1 point.

7.3.2 VERBAL RESPONSE: Examiner determines the best verbal response in accordance with the following response grading scale: a. The patient is oriented to person, place, and time --5 points. The patient can talk

and say who he is, where he is, the year, and the month. b. The patient is not oriented (is confused), but is able to communicate -- 4 points.

The patient can talk but is somewhat confused. c. The patient speaks in a disorganized manner (inappropriate speech) -- 3 points.

The patient does not enter into conversations but says understandable words (a curse, for example) or may say words which do not make sense.

d. The patient responds with moaning or groaning sounds (incomprehensible sounds) -- 2 points. The patient vocalizes (makes sounds) but does not say recognizable words.

e. The patient has no verbal response -- 1 point. The patient does not vocalize. He makes no sounds, nor does he respond to noxious stimulus.

7.3.3 MOTOR RESPONSE: Examiner determines the best motor response in accordance with the following response grading scale. a. The patient obeys commands appropriately and is able to move all extremities

equally and spontaneously -- 6 points. b. The patient is still able to obey commands, but exhibits weakness (for example,

drifting of an upper extremity) -- 5 points. c. The patient attempts to withdraw from the source of painful stimulus (flexor

withdrawal) -- 4 points. d. The patient flexes an extremity abnormally -- 3 points. e. The patient extends an extremity abnormally -- 2 points. f. The patient has no motor response to painful stimuli (flaccid) -- 1 point. NOTE: The Glasgow Coma Scale may not be valid in certain circumstances. The score of a patient who has used alcohol or other mind-altering drugs, is hypoglycemic, is in shock (systemic blood pressure less than 80 mm Hg), or who is hypothermic (body temperature below 34o C) may not accurately reflect the patient's level of consciousness.



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7.3.4 MEANING OF TOTAL POINTS ON GLASGOW COMA SCALE: The total points accumulated from the patient's responses indicate the following levels of consciousness:

Pict:40 Glasgow Coma Scale. (Abbreviated response scale)

1. Comatose. Less than 8 points on the Glasgow Coma Scale. 2. Moderate head injury. GCS total of 9 to 12 points. 3. Mild head injury. A total point count of 13 to 15 on the Glasgow Coma Scale.



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8.0 GENERAL MANAGEMENT OF HEAD TRAUMA:

8.1 PHYSICAL THERAPY:

Neurological Physical Therapy specializes in the evaluation and treatment of individuals with movement or functional problems due to congenital and/or acquired disease, trauma or dysfunction of the nervous system. Medically-Based Fitness works with a broad range of conditions including: Balance Deficits Parkinson's Multiple Sclerosis Brain Injury Spinal Cord Injury Peripheral Neuropathy Stroke Polyneuropathies Dizziness Vestibular Coordination

MBF Physical Therapy restores physical function and improves the efficiency of movement by addressing the individual client's functional limitations. Our therapists treat the functional deficits you have in order to improve your daily life. MBF takes an active approach in treatment, and problem solves long-term solutions with individualized programs treating the whole body. Our care is transferable to daily life activities making clients happier, healthier, and more independent. MBF Physical Therapists excel in treatment of the neurological system. MBF has been working with individuals with neurological impairments since 1996. There have been three Master's and two PhD degrees earned through research performed at Medically-Based Fitness. We utilize outcome based research and the most current research to guide our programming. We have concrete outcomes that improve the active approach to therapy in order to advance the life of every client.

8.2 PARKINSON'S SPECIFIC PROGRAMMING:

MBF is a resource to individuals with Parkinson's disease for information, education, and treatment. MBF Physical Therapy enables an individual to compensate for the changes brought on by Parkinson's disease by providing programming that is specifically developed for individuals limited by this disease. The treatment will include therapies to address immediate limitations and develop long term programs to promote functional independence through the disease process. The physical therapy includes education for the individuals and their caregivers.



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8.3 PHYSICAL THERAPY FOR PARKINSON'S ADDRESSES:

Balance and Coordination Gait Weakness Pain Posture Trunk and Joint Mobility Motor Programming Fatigue Immobility

8.4 PHYSICAL THERAPY FOR INDIVIDUALS WITH PARKINSON’S DISEASE:

The benefit of physical therapy and general forms of exercise in patients with Parkinson’s disease (PD) has been recognized for years. However, the traditional approach to physical therapy intervention for people with PD has been focused on teaching patients compensatory strategies to bypass the basal ganglia pathology. The use of external cues and cognitive strategies have been considered the practitioner's main training options. Thus, individuals with PD are instructed to consciously process movement information such as thinking about swinging the arms or taking large steps. In addition, the physical demands of many of the exercise protocols have been low to moderate in intensity. The goal of therapy has been largely to help people maintain what motor capability they have for as long as possible and to help them adjust as their functional level inevitably declines. This traditional approach to physical therapy intervention, i.e., teaching compensation for motor deficits, stems from the assumption that in the case of a neurodegenerative process such as that seen in PD, there is no potential for neurological recovery.

This assumption has been challenged by the demonstration of activity-dependent behavioral recovery, neurorestoration and neuroprotection associated with intensive physical training in animal models of PD.

8.4.1 EXERCISE-INDUCED NEUROPLASTICITY IN BRAIN INJURY:

One of the most exciting advances in neuroscience over the last 15 years has been the recognition that the brain's capacity for recovery from injury is far greater than previously thought. It is now recognized that the brain has the ability to reorganize (i.e., neuroplasticity) after disease or injury and that this phenomenon can be facilitated through activity-dependent processes including environmental enrichment, forced-use, complex skills training, and exercise. Most of our understanding of this activity-dependent plasticity is derived from studies of brain injury related to stroke and spinal cord injury. Lesion models (rodent and nonhuman primate) in the cortex have permitted investigation of neuroplasticity by studying the effect of forced active use on body segment(s) impaired by brain injury. In addition, basic science research has provided substantial evidence that functional locomotor recovery occurs in animal models of stroke and spinal cord injury when intense, locomotor training is employed. Noninvasive imaging and stimulation techniques now offer evidence that activity-dependent reorganization occurs in the human brain in response to exercise, locomotor training and motor skill learning. This activity-dependent plasticity has been shown to play a major role in the recovery of function after stroke. An important example of this is preliminary work using



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functional magnetic resonance imaging (fMRI) before and after treadmill training with body weight support (BWS). Use of body-weight-supported treadmill training (BWSTT) involves an overhead harness that can ease the transition into ambulation and eliminates the need for assistive devices (Figure 1). Because patients are protected from falling, BWSTT allows them to safely train at greater walking speeds. The intensive, task-specific practice of BWSTT promotes neural recovery rather than compensation as evidenced by significant improvements in velocity of locomotion, motor control of the hemiparetic limbs and alterations in fMRI activation patterns. Similar to studies of the injured spinal cord and cortex, work in the MPTP-lesioned (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson's disease has demonstrated that behavioral recovery and neuroplasticity of the injured basal ganglia may be modulated through high-intensity treadmill training. We found that central nervous system (CNS) neuroplasticity, in the form of both neurochemical and morphological adaptations, appears to underlie the observed behavioral recovery. In addition to our studies in the MPTP-lesioned mouse, other researchers have found evidence of enhanced neuroplasticity (behavioral and neurochemical) in the unilateral 6-OHDA-lesioned rat after forced use18. In this model of basal ganglia injury, rats were forced to exclusively use their affected limbs by means of ipsilateral limb casting. Casted animals showed increased affected limb use and increased expression of dopamine in the striatum compared to noncasted animals. These studies support the notion that intensive behavioral experience facilitates neuroplasticity in the injured basal ganglia. A neuroprotective effect of exercise was demonstrated when the ipsilateral forelimb was immobilized prior to the administration 6-OHDA. By immobilizing the limb that would not be affected by the neurotoxin, the rats were forced to exercise the forelimb that normally would be impaired when the toxin was injected. The results showed that the exercised limb, which should have been affected by the toxin, was not impaired. Additionally, this forced limb use prior to the 6-OHDA injection appeared to protect the dopaminergic neurons. In fact, 28 days after injection of the toxic compound, only six percent of dopamine neurons were lost in rats that had undergone forced use (i.e., exercise) before the injection, compared with a loss of 87 percent in rats that had not been forced to use one limb prior to the injection of the toxin.



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8.4.2 CURRENT APPROACHES TO EXERCISE IN PD: One of the most exciting areas in rehabilitation science is the translation of

exercise-induced neuroplasticity demonstrated in animal models of PD to human clinical trials. Whereas the goals of physical therapy intervention continue to include symptomatic relief, improved function and the general benefits of improved muscle strength, aerobic fitness, and balance, there is now an interest to determine the exercise parameters that will challenge impaired systems, promote recovery and modulate disease progression.

The potential neuroprotective effect of intensive exercise was recently revealed in a study by Chen et al., (2005). The objective of this study was to investigate whether greater physical activity is associated with a lower risk of PD. The authors prospectively followed 48,574 men and 77,254 women starting in 1986 who provided information on level of physical activity. During the follow-up, a total of 252 (male) and 135 (female) cases of PD were identified. It was found that strenuous exercise in early adult life was inversely related to PD risk in men. Compared with men who regularly exercised less than or equal to two months per year, those with greater than or equal to 10 months of strenuous exercise had a 60 percent lower PD risk. Similarly, in women, strenuous exercise in early adulthood tended to be inversely related to PD risk later in life.

Increasingly more exercise research in PD is investigating the effect of challenging, highly intensive exercise on functional improvement in this patient population. In addition, there is increasingly greater interest to identify the role of neuroplasticity as the underlying mechanism of exercise-induced functional improvement Hirsch et al., (2003) demonstrated that muscle strength and balance can be improved in persons with PD by high-intensity resistance training and balance training. Subjects undergoing ten weeks (three times a week) of high-intensity lower extremity resistance training and balance training were assessed before, immediately after training, and four weeks later. Muscle strength and balance increased substantially and this effect persisted for at least four weeks.

Zigmond and collaborators are currently conducting a study to determine the neuroprotective effect of different forms of exercise on individuals with mild PD symptoms. The subjects engage in exercise three times a week over a 12-week period. Exercise intensity and specificity is being manipulated in a variety of ways to see if any or all types of exercise are able to reduce the progression of the disease.

Recent literature has shown that individuals with PD can benefit from treadmill training in which gait behavior is driven more automatically and at significantly higher intensities. Three studies underscore the value of treadmill training as a treatment option for individuals with PD.

Pohl et al., (2003) examined the short-term effects of unsupported, speed-dependent treadmill training on patients with early PD. Significant, immediate differences were observed following a single treadmill training intervention versus conventional gait therapy in both walking speed and stride length.

In two separate randomized, controlled trials Miyai et al, compared immediate and long-term effects of two interventions for individuals with Parkinson's disease. The interventions were BWSTT and a standard physical therapy regimen involving general conditioning, range of motion, and gait training exercises. After 12 treatment sessions, the BWSTT group exhibited significantly greater changes in disease severity ratings as



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determined by the Unified Parkinson’s Disease Rating Scale (UPDRS), whereas the conventional therapy group showed negligible differences. Furthermore, both velocity and cadence over a distance of ten meters improved post-treatment in the BWSTT group, which persisted even after a four-week period of no training.

Clearly, the potential gains through treadmill training for individuals with PD are remarkable. However, the specifics of what actually occurs in the structures of the brain to improve gait and motor performance are not yet known. Currently, researchers from the Department of Biokinesiology and Physical Therapy at the University of Southern California are investigating the underlying neural processes by which BWSTT promotes functional changes in individuals with early-stage Parkinson's disease. As stated above, evidence now exists that functional improvement and activity-dependent neuroplasticity can result from the high-intensity, task-specific experience of BWSTT in animal models and patients with stroke and spinal cord injury. While Miyai et al., demonstrated that this intervention also leads to functional performance improvements in patients with PD, the neural mechanisms supporting the improvements were not examined. Based on animal models that have linked neuroplasticity with high-intensity intervention for subjects with PD, we believe that the performance improvements in PD are also, at least in part, driven by neuroplasticity. We think BWSTT is the most promising method for inducing neuroplasticity in individuals with Parkinson's disease in part because of the results we have seen in our mouse model. Additionally, this method combines some of the most critical characteristics of practice that have been identified as facilitating activity-dependent plasticity: higher intensity than the individual is capable of on his or her own gained through the velocity of the treadmill; high repetition through multiple steps; active engagement on the part of the individual; and the sensory experience of normal gait kinematics.

To date, no systematic study has examined the effect of high-intensity exercise on functional outcome in PD and its underlying mechanism (neuroplasticity of the dopaminergic system). Our interest is to fill the existing gap in the literature and to test our hypothesis that humans with PD are subject to neuroplasticity and behavioral recovery through activity-dependent processes when provided with high-intensity training. By understanding the effects of exercise on neuroplasticity, novel nonpharmacological therapeutic modalities may be designed to delay or reverse disease progression in idiopathic Parkinson's disease.



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8.5 VESTIBULAR THERAPY:

What is Vestibular Therapy? Vestibular therapy encompasses a multitude of diagnoses and subjective complaints. A vestibular therapist can effectively treat patients who are dizzy for reasons including Benign Paroxysmal Positional Vertigo (BPPV); Vestibular Hypofunction or Injury; Meniere's Disease; as well as general imbalance, fall risk, deconditioning, and neurological injuries such as MS, TBI, or concussion with resultant complaints of dizziness.

The treatment received will vary depending on the etiology/cause of the patient's complaints. Some patients are seen only a few visits and are symptom-free very quickly. Other patients have to be seen for a longer duration of time, but will also notice dramatic changes in their subjective complaints, dizziness, or imbalance; as well as in objective measures.

Why should you choose a Certified Vestibular Rehabilitation Specialist? This is an area of study requiring greater focus and time than is typically devoted in the

entirety of physical therapy education. A Vestibular Rehabilitation Specialist is trained to screen patients for other causes of their symptoms and is able to recognize situations in which the patient may not be appropriate for therapy. Also, Vestibular Therapists have a greater understanding of the complex workings of the Vestibular and Balance systems, allowing them to more appropriately focus their treatments toward fixing/modifying the symptoms to allow for maximum outcomes. Follow these general principles in managing patients with possible head trauma: a. Focus on maintaining adequate oxygen and cerebral blood flow. b. Hyperventilate (increased amount of air) to decrease the increased intracranial pressure

and prevent brain stem herniation by causing vasoconstriction (narrowing of blood vessels).

c. Maintain an airway. This is critical since the injured brain has increased oxygen demands. d. Prevent coughing, bucking, seizing since any of these will raise intracranial pressure. e. Intubate early, if possible, since a head trauma patient will frequently aspirate (intake of

foreign material into the lungs during the act of breathing). f. Protect the cervical spine. g. Prepare to suction. Patients with head injuries often vomit. h. Control bleeding and reestablish circulation.

NOTE: If direct pressure is used to control scalp wounds, remember to press only on a stable skull.

i. Be alert for shock. Start an IV of lactated Ringer's solution to keep a vein open and adjust the rate to the patient's needs.

j. Be observant of possible internal injury. Shock without gross bleeding will not be caused by brain injury except at the terminal stage. The patient may have internal injuries.

k. Head injury with multiple trauma should be managed the same as any other patient in shock. Establish an IV with an electrolyte solution and use a pneumatic antishock garment such as MAST, if necessary and appropriate to control bleeding.

l. A patient with only a head injury should be fluid restricted to decrease cerebral edema. m. Anticonvulsants may be required. n. Document carefully. Describe the patient's condition in terms of responsiveness to the

environment. NOTE: Avoid words such as lethargic, semiconscious, obtunded (to diminish pain or to diminish touch sensation).



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People who have suffered TBIs may have lost the ability to do certain movements, feel certain sensations, and speak properly. They will need physical therapy to re-train movements and sensations so that they can get back as many of these activities as possible. The chance of getting these lost movements back with physical therapy depends on the age of the individual, the severity of the injury, and the amount of time that they were unconscious following the injury. Many behavioral changes usually accompany TBIs. What these changes are depend on where the injury occurred in the brain. Some changes may be irritability, a decreased ability to reason, a decreased concentration, forgetfulness, and personality changes. Some of these changes may get better with time.



TRAUMA AND DISEASE



9.0 PREVENTION STRATEGIES:

There are many ways to reduce the chances of a traumatic brain injury (TBI), including:

1. Wearing a seat belt every time you drive or ride in a motor vehicle. 2. Buckling your child in the car using a child safety seat, booster seat, or seat belt (according to the

child's height, weight, and age). Children should start using a booster seat when they outgrow their child safety seats (usually

when they weigh about 40 pounds). They should continue to ride in a booster seat until the lap/shoulder belts in the car fit properly, typically when they are 4’9” tall.

3. Never driving while under the influence of alcohol or drugs. 4. Wearing a helmet and making sure your children wear helmets when:

Riding a bike, motorcycle, snowmobile, scooter, or all-terrain vehicle; Playing a contact sport, such as football, ice hockey, or boxing; Using in-line skates or riding a skateboard; Batting and running bases in baseball or softball; Riding a horse; or Skiing or snowboarding.

5. Making living areas safer for seniors, by: Removing tripping hazards such as throw rugs and clutter in walkways; Using nonslip mats in the bathtub and on shower floors; Installing grab bars next to the toilet and in the tub or shower; Installing handrails on both sides of stairways; Improving lighting throughout the home; and Maintaining a regular physical activity program, if your doctor agrees, to improve lower body

strength and balance. 6. Making living areas safer for children, by:

Installing window guards to keep young children from falling out of open windows; and Using safety gates at the top and bottom of stairs when young children are around.

7. Making sure the surface on your child's playground is made of shock-absorbing material, such as

hardwood mulch or sand.

PTP&M004 PTM of Central Nervous System trauma and disease Medical Journal

Health & Medicine

nervous system diseases

spinal cord trauma

subject matter

spinal cord injury

disease notice

authorized agent

proprietary information

revision historyrev