Medical and Physical Complications

Section 3

THE ESSENTIAL

BRAIN INJURY

GUIDE

Presented by: Bonnie Meyers,

CRC, CBIST

Director of

Programs &

Services

Brain Injury

Alliance of

Connecticut

Certified Brain Injury Specialist Training

This training is being offered

as part of the Brain Injury

Alliance of Connecticut’s ongoing commitment to

provide education and

outreach about brain injury in

an effort to improve services

and supports for those

affected by brain injury.

Presented by Brain Injury Alliance of

Connecticut staff:

Rene Carfi, MSW, CBIST

Senior Brain Injury Specialist

Bonnie Meyers, CRC, CBIST

Director of Programs & Services

ContributorsDavid Anders, MS, CCC-SLP, CBIS

Helen Carmine, MSN, CRNP, CRRN

Heather Ene, MD

Lawrence Horn, MD

Susan Ladley-O’Brien, MD

Emily McDonnell

Mary Pat Murphy, MSN, CRRN, CBIST

Grace Nolde-Lopez, NP

Denise R. O’Dell, PT, DSc, NCS

Jennie L. Ponsford, BA, MA, PhD, MAPsS

Benjamin Siebert, MD

ACBIS Exam Study Outline

Medical Issues

Autonomic storming

DVT/PE

Bladder issues

Aspiration

TBI and spinal cord overlap

Seizures, complications, and mortality

Cranial nerve damage

Pain after brain injury

Evaluation and treatment of headaches

Keep

an eye

out for

this

ACBIS Exam Study Outline

Physical Issues

Spasticity, hyperreflexia, contractures, HO

Pressure sores

Perceptual deficits

Complications related to aging

Disorders of Consciousness

Prevalence and types of DOC

Prognosis and medical management of DOC

Importance of autonomic nervous system

Keep

an eye

out for

this

ACBIS Exam Study Outline

Sleep and fatigue disorders

Causes, measurement, persistence, and treatment of

sleepiness/fatigue

Fatigue VS sleep disruptions

Psychological fatigue

Keep

an eye

out for

this

Medical Complications

Gain an understanding

of medical

complications

frequently seen in

persons with brain

injury

Be able to articulate the common

issues related to elimination in the

TBI population

Be able to describe dysphagia and theimportance of tube feeding in persons

with brain injury

Be able to discuss

prevention and treatment of pressure

sores

Be able to distinguish between epileptic

seizures and post-traumatic seizures

Know the symptom clusters of different

types of headaches frequently observed

in the TBI population and appropriate

treatments for each

Brain Injury and Body Systems

CARDIOPULMONARYComplications involving the heart (cardiac) and breathing (respiratory)

Can occur immediately, chronically, or emerge as late complications

Associated with increased mortality and morbidity

Ventilator

Trach.

Meds –Maintain

adequate

BP and cerebral

Blood flow

Either by direct traumato organs themselvesOr to parts of brainThat control heart/lungfunction

Clustering of

Blood Cells

Chronic Cardiopulmonary Issues

Orthostatic

hypotension

Aspiration

pneumonia

Deep vein

thrombosis

Blockage

Develops

Part of Blockage Breaks Free

Etiology of

DVT

Dysautonomia

Sometimes called “autonomic

storming”

Generally at lower level of neurological

activity GCS 3-8

Heart/respiratory rates

Blood pressure

Temperature

perspiration

dystonia - abnormal muscle tone/postures

Usually resolves in early recovery

Cardiovascular and Pulmonary

Monitoring Monitor heart rate: 60-90 beats per minute

Monitor blood pressure: 100/65-137/84

Monitor respirations: 12-20 breaths per minute

Observe for light headedness and dizziness

Listen for cough, congestion, difficulty breathing, fever

Look for leg swelling (DVT) usually only on one extremity

MUSCULOSKELETAL

COMPLICATIONS

Fractures,

dislocations,

spinal peripheral

nerve injuries –

initial trauma

Neurologically-

based

complications

Reflexes, sensory

Integration, ROM,

muscle tone,

strength,

endurance,

postural control

Heterotopic Ossification – abnormal growthOf bone in soft tissues adjacent to joints

Hyperreflexia – involuntary exaggerated deep tendon reflexes

Spasticity – involuntary increase muscle tone

Contractures – abnormal, usually permanent, condition of joints – decreased

ROM, often in flexed position and fixation

due to wasting away/shortening of muscle

fibers and loss of skin elasticity

Identification and

Management of Chronic

and Late Emerging

Complications

Impact of normal aging/degeneration considerations (Osteoporosis, osteoarthritis)

Normal aging/degeneration

and re-emerging long term

consequences of trauma

TX – Spasticity/contractures = exercise, casting, orthotic

Interventions, ultrasound, e-stim to improve flexibility/tone

oral anti-spasticity meds, nerve blocks, botox,

Orthopedic mngt, surgically implanted baclofen pump

Musculoskeletal problemsImpact one another, createNew problems – postural control,Balance, and pain

ELIMINATIONBowel/Bladder Function

Caution: Do not Assume incontinenceIs behave. issue that is intentional/volitional

Urinary Incontinence Management

Signs of UTI – 60% indiv. within

6 weeks of injury

Frequent/painful urination

Fever

Possibly increased

agitation

Possibly decreased level of

alertness

Decreased awareness of bladder

needs, poor tone, less holding

capacity, increased sense of

urgency

Interventions: timed voiding, absorbent

Briefs, minimize caffeine (bladder irritant),

Catheters (risk for infection)

Bowel and Fecal Incontinence

ManagementRisk Factors:

Neurological issues (SPI)

Mobility

Food consistency and intake status

Medication and impact on

gastrointestinal motility

Management:

Stool softeners, bulk laxatives,

Suppositories, enemas, other cathartics

Regular toileting schedule (2-3 days) to

Promote bowel emptying

GASTROINTESTINAL

need to achieve and maintain

adequate nutritional status

Regulation of

Hypothalamus,

Parasympathetic

sympathetic

systems

Cortical functions

Arousal,

dysphagia, safety

awareness,

medications.

chronic issues:

reflux (GERD)

Weight mngt.

Early Issues: Nutrition

and Feeding

Metabolism increases following

Mod-severe injury – 40% more

Calories – may be long term need

Initial nourishment via

parenteral/IV support

and/or tube feedings

supplement nutrition

dysphagia

G-tube = surgically

Placed into stomach

Or small bowel

J-tube – through skin

Of abdomen into

Midsection of

small intestine

Chronic Issues: Swallowing

Monitor swallowing programs prescribed by therapist (types of food and/or liquid permitted, level of supervision)

Monitor for coughing while eating or drinking

Monitor weight loss and dehydration

May need to offer fluids

Aspiration RisksPulmonary/lung aspiration - Breathing a foreign substance into your. The substance could be food, liquid, medicine, mucus, or saliva.

Choking OR aspiration pneumonia, which is a serious infection in the lungs

Swallowing Process

Phase 1 is the oral preparatory/oral

stage which includes mastication,

bolus formation, and propulsion of

the bolus into the pharynx

Phase 2 is the pharyngeal phase which

includes movement of the bolus past

the epiglottis, through the pharynx, and

past the upper esophageal sphincter

Phase 3 is the esophageal phase

where the bolus moves through

the esophagus toward the lower

esophageal sphincter

Swallowing is a complicated

process, and dysfunction can

lead to aspiration

A study that examined severe

TBI found disorder rates of 90%

early after injury

65% had problems in the Oral

Phase; 73% in the pharyngeal

phase

National Dysphagia Diet Levels: Food

National Dysphagia Diet Levels:

Liquids

Thick-It can be used to change consistency of liquids

METABOLIC/

ENDOCRINE

Diabetes Insipidus/ Metabolic

and Endocrine DisordersIndividuals may present with

Metabolic syndrome

Hypothalamic-pituitary changes

Growth hormone dysfunction

Hypopituitarism

Gonadotropin deficiency

These problems tend to be diagnosed a year or more post-injury and occur in up to 30% of individuals with moderate-severe injuries who are greater than one year post injury

Implications:

weight mngt.

sexual dysfunction

osteoporosis

decreased muscle/strengthDI – decreased vasopressin, fluid levels

med - desmopressin

REPRODUCTIVE

SYSTEM

Reproductive Health Challenges

UTIs, depression, osteoporosis

Endocrine disorders, dysmenorrhea

Polycystic ovarian symptoms

INTEGUMENTARYOrgan system includes skin/appendages

Body’s largest organ system

Wounds

Abrasions

Lacerations

Pressure sores

Skin integrity

Hygiene

Turning sched.

Proper fitting

Inspection

Fungal and

bacterial

infections

Acne

Sweating

Rashes

Pressure Sores

Pressure sores can be prevented by:

Keeping skin clean and dry

Changing position every two hours

Using pressure-relieving devices both

preventatively as well as after the

development of a pressure ulcer, including:

Specialty mattresses

Specialty cushions

Pressure-relieving tilt-in-space

wheelchairs

Risk: decreased mobility, incontinence, poor

nutrition, spasticity, sensory impairment

Areas of bony prominence

shoulders

elbows

lower back/buttocks

hips, inner knees

heels

Occurrence correlated with

dependence on others for ADLs

STAGE I – intact skin

Intact skin with non-blanchable redness of

a localized area usually over a bony

prominence. Darkly pigmented skin may

not have visible blanching; its color may

differ from the surrounding area. May

indicate “at risk” persons. No open sores.

STAGE II – skin breaks open

Partial thickness loss of dermis presenting

as a shallow open ulcer with a red pink

wound bed, without slough. May also

present as an intact or open/ruptured

serum-filled or sero- sanginous filled

blister. *bruising indicates deep tissue

injury.

STAGE III – deep wound

Full thickness tissue loss. Subcutaneous fat

may be visible but bone, tendon or muscle

are not exposed. Slough may be present

but does not obscure the depth of tissue

loss. May include undermining and

tunneling.

STAGE IV – very deep, tissue loss

Full thickness tissue loss with

exposed bone, tendon or muscle.

Slough or eschar may be present.

Often includes undermining and

tunneling.

UNSTAGEABLE

Full thickness tissue loss in which

actual depth of the ulcer is completely

obscured by slough (yellow, tan, gray,

green or brown) and/or eschar (tan,

brown or black) in the wound bed.

DEEP TISSUE INJURY

Purple or maroon localized area of

discolored intact skin or blood-filled

blister due to damage of underlying soft

tissue from pressure and/or shear. The

area may be preceded by tissue that is

painful, firm, mushy, boggy, warmer or

cooler as compared to adjacent tissue.

Stages of Pressure Ulcers

COMMON

INFECTIONS Individuals with brain injuries are susceptible to infection when they have open wounds, use in-dwelling devices, or are immuno-suppressed

UTI – More than 60%

have UTI within 6 months –

can lead to urosepsis

Infection associated with

Neurosurgery in 50% people BI

Cellulitis-bacterial skin infection

Meningitis – inflammation and

Swelling of protective

membranes brain/spinal cord

Neurologic

Complications

Seizure Pain

Headache

Seizures

The segregation of seizure

events according to time of

appearance after the initial impact is based partially upon

the observed future risk of

seizure reoccurrence and ideas

regarding the physiological

events that underlie their

emergence

Immediate post-traumatic convulsions (IPTC) Within moments of injury –considered by most to represent non-epileptic events. Associated

with low risk for recurrent seizures

Occurrence

ranges from

4-53%

After TBI, individuals are 22 times more likely to die of a

seizure disorder as compared to the general population

Abnormal disorderlyDischarge electricalActivity in nerve cellsOf brain

Early Post-Traumatic Seizures (EPTS)

Severe brain injury

Depressed skull fracture

Penetrating head injury

Hematomas

Cortical contusion

Post traumatic amnesia > 24 hours

Chronic alcohol use

Children and adolescents

Detection and treatment of

EPTS are necessary in order

to minimize the potential for

secondary brain damage

The occurrence of EPTS is a

strong risk factor for the

development of late post-

traumatic seizures (LPTS)

RISK FACTORS

1 week or earlier after injury

Late Post-Traumatic Seizures (LPTS)

Similar to those for EPTS,

although LPTS are less

frequently seen in children

and more frequently seen in

people > 65 years of age

The strongest risk factors for

LPTS are missile wounds,

bilateral or multiple

contusions and multiple

craniotomies

Strong predictor of recurrent

seizures

RISK FACTORS:

Later than 1 week after initial head trauma

Status Epilepticus

The Epilepsy Foundation

has revised the definition of

Status Epilepticus to include

seizures that last too long

(any seizure lasting longer

than 5 minutes), as well as

those so close together

that the person does not

recover from one before

another begins.

Status epilepticus carries a

high mortality risk

Benzodiazepine - 1st line of tx – provide

Rapid seizure control

Seizure First Aid Do not force any object into the

person’s mouth or try to hold the

tongue

Clear the environment of harmful objects

Ease the individual to the floor to prevent injury from falling

Turn the person to the side to keep the airway clear and allow saliva to drain from mouth

Put something soft under the headand along bedrails, if in bed

Loosen tight clothing around the neck

Seizure First Aid Do not attempt to restrain the person

Do not give liquids during or just after the seizure

Continue to observe the person until fully alert, checking vital signs such as pulse and respirations periodically

Give artificial respiration if person does not resume breathing after seizure

For Status Epilepticus call 911 within 3-5 minutes or based on physician recommendations

For Seizures that are prolonged or different than a person’s normal baseline seizure, call 911

Practical Implications of Seizures

Increased mortality

Increased morbidity

Risk of injury

Can lead to disability

Impacts employment

Impacts driving

Seizure Treatment

Prophylaxis - For adult patients with severe TBI, prophylaxis with phenytoin for 7 days is effective in decreasing the risk of early post-traumatic seizures.

Continuing antiepileptic prophylaxis (phenytoin, carbamazepine or valproate) beyond one week has not been shown to be effective in decreasing the risk of late post-traumatic seizures

Levetiracetam is also used prophylactically

Status Epilepticus Benzodiazepines are first line treatment for this

condition, as they provide rapid seizure control.

PAIN

PAINNon-headache

Nocioceptive

Neuropathic

Post-Traumatic

Headaches

tensioin

craniomandibular

cervogenic

Migraines

Acute or Chronic

Subjective

Can have significant implications on

rehabilitation process and daily living

General Pain can be in the form of orthopedic

injury/musculoskeletal, headache, pain

due to spasticity and contracture,

heterotopic ossification, myofascial

pain, neuropathic pain or pain related

to other medical conditions

Pain can disrupt the rehabilitation

process with restlessness, agitation,

non-compliance and sleep

disturbances

After the event, multiple fractures, internal injuries, and shoulder injuries often produce acute pain symptoms

Over time, neuropathic pain secondary to nerve injuries, subluxation, tendinitis, and pain due to spasticity may emerge

Pain experiences can be subjective and can be acute or chronic

Management – team approach, tx. Plan with goal of stabilization & mngt.

Daily activities to include balance rest, activity, sleep

Non-Headache Pain

Pain related to the peripheral nerve fibers

Pharmacological treatments include:

NSAIDS - aspirin, ibuprofen, naproxen

Acetaminophen

Topical agents

Anti-spasticity medications

Opioids

Pain associated with primary lesion of dysfunction of the nervous system

Medications to treat neuropathic pain in persons with TBI include

Topical agents, opioids, tramadol, Lyrica, anticonvulsants and antidepressants

Tricyclics (a category of antidepressants)

Interventional techniques including trigger point injections, nerve blocks and epidural steroids may also prove to be effective

Nocioceptive Pain Neuropathic Pain

The most common pain pathways in persons with TBI are nocioceptive and

neuropathic, requiring different pharmacologic approaches

Damage to tissue – sharp, aching, throbbing Damage to the nerves

Post-traumatic Headache Intl. Headache Society – commences within 14 days regaining consciousness

A primary headache has no

specific cause

A secondary headache may

have an identifiable cause

that can be determined

A chronic headache is one that occurs at least 15 days per month for at least 3 months

A chronic headache cannot be linked to overuse or withdrawal of medication

Primary or Secondary Acute or Chronic

Two important designations in this classification system are whether the

headaches are primary or secondary, and whether they are acute or

chronic headache

mTBI -95% mod-severe TBI 22%PTH -

Migraine

Tension Type

Headache

(TTH)Cervicogenic

Cranio-mandibular

Types of Post

Traumatic

Headache

Tension Type Headache (TTH) Headache is bilateral

head pain of pressing

quality, much like that of

a tight hand or vice

clamping across the head

Occurs from either a neck

or head muscle strain or

injury

Does not get worse with physical activity and patients do not present with other symptoms like sensitivity towards light, sound and taste

NSAIDs/acetaminophen

antidepressants

Low load craniocervical mobilization-long term mngt.

Botox (prevents muscle contractions)

Craniomandibular Headache

Defined as a subtype of tension type headaches associated

with the temporal mandibular joint

Can be very debilitating

causing patient to have

difficulty with eating and

talking, which require

movement of the jaw and mouth

Conservative TX – dietary changes

Cervicogenic Headache Defined as a head pain generated from the

cervical spine

A clinical diagnosis can be made clinically

(provoking the headache by manipulation),

or by nerve block

Nerve block is preferable as it the best

diagnostic method and can eliminate other

types of headaches which can mimic this

type of headache

Nerve injections/freeing nerves effective short term

Nerves are severed by burning them – long term

MIGRAINE4 stages

With or without aura

Noise

Touch

Smell

Light

Usually effects only one side, but not always

Usually not in the back of head

Migraine Phases Tend to occur as episodes of headaches that may have

different phases

Wolff’s Headache and Other Pain 8th ed., states that there are

four phases of migraine:

Prodrome Aura Headache Postdrome

Early SymptomsPhy/mental changes

Food cravings, mood changes

1-24 hrs

Symptoms that

follow headache

Hours/days to

resolve. Similar to

Prodrome stage

Neurological sympt.

numbness/tingling

vertigo

Speech/hearing

Throbbing, worse by

Movement, nausea

Vomiting, light/sound

Sensitivity

Usually peaks within 24Hrs (range 4-72)

Abortive- initially, combination aspirin, acetaminophen, caffeine (AAC). Otherwise,

triptans, NSAIDs, ergot derivatives, atypical antipsychotics, narcotics

Preventative-Tricylic antidepressants (serotonin re-uptake inhibitor)Topiramate (inhibits firing of neurons of trigeminal nerve

beta-blockers

calcium channel blockers

Treatment of Migraines

No longer thought to be simply

dilation/constriction of blood vessels

Neurological disorder involving nerve

pathways and brain chemicals

Headache Symptoms

haracter – sensation and intensity (throbbing, etc.)

nset – pattern to timing (morning, triggers)

ocation – where does it start? – does it radiate?

uration and frequency

xacerbation – what intensifies the headache

elief – what reduces the headache

COLDER

Used for

all headaches

PHARMACOLOGICAL

TREATMENT OF BRAIN

INJURY

Facilitating or

inhibiting

Neurochemical

transmitter

activity

Behavior/mood

Anxiety

Depression

Cognition

Med/phy. issues

Brain Injury Specialists and

Medications

Evaluate medication

efficacy

Observe side effects

Facilitate proper

administration

… and ask questions

FIRST AID

and other procedures

Standard Precautions

Approach to infection control which helps to prevent transmission of

blood-borne pathogens – universal precautions

Physical Complications

Be familiar with motor learning

principles

Gain an understanding of various

presentations of hydrocephalus, appropriate treatments, and the

risks involved in the treatment

Be able to distinguish between the standard

of care for lower extremities as opposed to upper extremities in patients with severe

spasticity

Be able to describe typical treatments for

heterotopic ossification and

deep vein thrombosis

Be able to articulate the 5 types of coordination

disorders common to persons with TBI

Be able to discuss the specific needs

of a person with concomitant TBI

and SCI

Learning

Objectives

Based on principles of:

Common language

motor learning

Strategic approach

Understanding of common co-

existing conditions after ABI

Motor Learning PrinciplesSet of internal processes associated with practice &

experience which leads to permanent skill development

and new behavior – Results in changes in central

nervous system that allows for production of new motor

skill

Stages of Motor Learning

Cognitive (What to do) acquires knowledge to perform task – think, plan, understand – conscious level

Associative (How to do) – begins to apply and self monitor – refinement with repetition, feedback – conscious and automatic

Autonomous (How to succeed)- refinement -consistently self regulates/self corrects. Refinement and less cognitive process involved

Motor Learning: Considerations for

Treatment Design

Performance – repetition of task

Generalizability – similar task

Resistance to contextual change – multiple/new environments

Guidance – therapist physically assisting to achieve desired movement

Feedback – intrinsic / extrinsic

Practice type – sequencing of

presenting information

Environmental influences on

motor learning – open or

closed environment

MEDICAL OR OVERALL

SYSTEM

COMPLICATIONS

HYDROCEPHALUS Spasticity Hydrocephalus

Heterotopic

Ossification

Vascular

Thrombus/

Emboli

Types of Hydrocephalus (2/3 mod-severe)

Obstructive/non-communicating – obstruction/blockage of cerebral

spinal fluid (CSF) – increased pressure, risk for poor outcome

Hydrocephalus ex-vacuo – brain tissue causes neuronal loss, brain

tissue shrinkage, brain atrophy, pressure usually normal

Surgical placement of a shunt to promote flow of CSF; careful

monitoring is required. – Complications for malfunctioning shunt:

fever, neck stiffness, changes in alertness

Types of Hydrocephalus – abnormal level cerebrospinal fluid

within ventricles

Treatments

Spasticity – motor disorder, velocity

dependent increase in tone

Damage to upper

Motor neurons Triggered by minimal

Movement of limb

Stretching

Spasticity ManagementMultimodal approach to treatment

• Medications –anti-spasmodics(Baclofen, dantrolene, diazepam, tizanidine)

baclofen pump, botox,

• Occupational and physical therapists

Goal: optimize recovery and reduce disability

Minimize Secondary Complications:

contractures, skin breakdown

Remove noxious stimulus (cold)

Heterotrophic Ossification (HO)

HO - formation of new bone

around joints as a consequence

of trauma and/or immobility

Surface around joint red/swollen,

increased pain, decreased ROM

is most common indicator

Interventions: meds (etidronate

disodium or NSAIDS)

Surgery – after bone has matured

Vascular Thrombosis

Deep vein thrombosis (DVT)occurs when a blood clot (thrombus) forms in one or more of the deep

veins in your body, usually in the leg

Deep vein thrombosis can cause leg pain or

swelling, redness, or fever but may occur without

any symptoms

Occurs often after immobility

Prophylaxis includes anti-coagulants like Heparin,

Lovenox or Coumadin

Without prophylaxis, a pulmonary embolus (PE) or

clot to the lungs can occur; this may interfere with

breathing and can lead to death

Thrombus

The rates of Deep Vein

Thrombosis (DVT) is as high as

54% in persons with TBI

Pulmonary embolism is the 3rd

leading cause of death in those

who survive the first day

Embolus

COMPLICATIONS WITH

SENSORY SYSTEMS OR

MOVEMENT

Cranial Nerve

Dysfunction

Somatosensory

Issues

Functional

Movement

Dysfunction

Cranial Nerve Dysfunction

Visual Disturbance

Facial drooping

Postural instability

Dysphagia

Autonomic dysregulation

Anosmia – loss, decrease smell

12 nerves emerging directly from

Brain/brain stem

Relay information from brain to parts of

Body (head/neck)

Somatosensory

Issues

Complex system of sensory

neurons/pathways that

responds to changes at

surface or inside of body

system sends nerve

impulses regarding:

• proprioception

• tactile sensation

• thermal sensation

• pressure sensation

• pain

Damage to right side of brain OR

parietal/occipital lobes

Functional Movement DysfunctionFunctional movement dysfunction creates problems

with:

Overall mobility – bed mobility,

transfers, gait, balance

Object manipulation –

reaching, grab/release, one/both hands

Implications for independence

Coordination DisordersInterlimb Coordination – damage to corpus

callosum, upper extremities, bimanual

coordination, timing, sequencing

Ataxia – cerebellum / voluntary movements,

decreased coordination

Athetoid – slow, involuntary, convoluted writhing

movements, fingers, toes, hands, feet

Ballisms – quick, flailing movements

Choreiform – continuous, rapid, unpredictable

movements

Tremors – unintentional trembling

Visual

Perception orInterpretation

Deficits

Visual Acuity

Agnosia

Spatial Relations

Body Schema

Common after brain injury

Very complex system, integrated W/

All other systems of brain/body

Terms of Visual Function

Visual Function Description

Visual acuity Clarity of vision (Snellen chart for testing)

Eye movements Tracking, saccades, smooth pursuit, fixation

Visual fields Zone of vision, central v peripheral and

quadrants

Binocular vision Left and right eye move together (conjugate)

Vergence Eyes symmetrically turn inward/outward for

adjustment to varying object distances

Vestibular

interactions

Vestibular-ocular reflex (VOR) to maintain

gaze during head turning

Perception or Interpretation Disorders

Body Schema/ Body Image

Disorders Unilateral neglect – unable to

attend to/comprehend one side

of body

Anosognosia – deficit of awareness

Right/left discrimination

Somatognosia – unaware body part

Agnosia - recognition

• Visual Object Agnosia

• Auditory Agnosia

• Tactile Agnosia

Apraxia – motor planning

• Ideomotor – model, imitate,on

command

• Ideational-command/automatically

Conceptually using objects

• Buccofacial –purposeful movements

lips/tongue, larynx, cheeks

More Perceptual

Deficits

Spatial Relation Disorders

• Form discrimination – if in different orientation or objects close in shape

• Spatial relations disorder – relationships between objects or oneself and object, crossing midline

• Vertical disorientation – difficulty sustaining upright position, posture for balance

• Depth and distance perception –difficulty judging depth/distance

Figure ground

discrimination: cannot determine

a figure from its

background

Vision Issues

Visual system one of the most

complex systems of brainPhotophobia

Double Vision

(Diplopia)

Visual field loss

Decreased acuity

Photophobia (light sensitivity)

Contrast sensitivity

Diplopia

CONCOMITANT TBI

AND SPINAL CORD

INJURY (SCI)

60% people

with spinal

cord injury

also have

brain injury

Concomitant TBI and SCI

SCI annual incidence is

approximately 12,000 new cases

annually, or 3.1/100,000

TBI present in 60% of individuals

with SCI

Complete injury = almost all or all feeling (sensory) and all ability to control movement (motor function) are lost below the spinal cord injury

Incomplete injury = feeling (sensory) and or ability to control movement (motor

function) is partially preserved

Paralysis of the body below the level of the spinal cord injury;

Paraplegia - trunk, legs and pelvic organs are affected (paralyzed)

Tetraplegia - arms, hands, trunk, legs and pelvic organs are all affected

(paralyzed)

Incidence SCI Injury Description

SCI: Considerations

Skin Care needs – Vulnerable to pressure

sores because lack of sensation and pressure over bony prominences

Monitoring and repositioning every 2 hours

Bowel Care needs – controlled by sacral

spinal nerves

Bowel program

Bladder Care needs/goals Bladder management for UTI prevention, maintaining low residuals in bladder, and continence

Disorders of Consciousness

Learning

Objectives

Be able to describe the appropriate use of goal-setting for

the person with DOC

Be able to provide

examples of the modalities of sensory

stimulation

Distinguish between diagnostic criteria for

coma, vegetative state, and minimally

conscious state

Gain an understanding of

disorders of consciousness

(DOC)

Be able to articulate the methods of

medical management for the

person with DOC

Be able to identify the methods of

physical management for the

person with DOC

Disorders of ConsciousnessClassification System: 3 generally accepted levels

Minimally Conscious (MCS)

Vegetative State (VS)

incidence - 4,200/year

Estimated 315,000 persons living with DOC in U.S.

Brain

death

and

“locked

in” not

DOCPrevalence

Disorders of Consciousness Occurs with injury to:

Reticular Activating System (RAS) (Arousal)collection of primitive structures and nerve pathways

Arousal-primitive & involuntary response to internal & external stimuli

Higher cortical areas in the cerebrum (Awareness)

Awareness-ability to receive & process sensory information – related it to environment/make sense of information. Regulated by higher cortical areas in cerebrum.

influences muscle tone, breathing,

blood pressure, and wakefulness,

basic biological rhythms

Disorders of ConsciousnessDOC

Subcategory

Arousal Awareness Prevalence

Coma No No Weeks

(2-4 wks)

Vegetative

State

Yes No Months to

years

Minimally

Conscious

State

Yes Fluctuates Months to

years

Emergence from DOC – clinically out of DOC if meet 1 of 2 behavioral criteria –functional communication verbal/gestural to yes and no questions

OR functional use of 2 or more objects (cup/toothbrush)

Diagnostic Criteria: Coma

No arousal/eye-opening (no

sleep/wake cycle)

No behavioral signs of

awareness

Impaired spontaneous breathing

Impaired brainstem reflexes

No vocalization > 1 hour

Coma usually resolves in 2-4 weeks with the individual passing

away or resolving into VS or MCS

Diagnostic Criteria: Vegetative State

Arousal/spontaneous or stimulus induced eye opening (sleep/wake cycle)

No behavioral signs of awareness

Preserved spontaneous breathing

No purposeful behaviors

No language production or comprehension

Preservation (partial or complete) of hypothalamic and brain stem autonomic functions

May grimace to pain, localize to sounds inconsistently

Atypical: visual fixation, response to threat, inappropriate single words

Diagnostic Criteria: Minimally Conscious

State Arousal/spontaneous eye-opening (sleep/wake cycle)

Fluctuating but reproducible behavioral signs of awareness

Response to verbal directive

Environmentally-contingent smiling or crying

Object localization and manipulation

Sustained visual fixation and pursuit

Verbalizations

Intentional but unreliable communication

Emergence from MCS:Communication (verbal or gestural yes/no)

Use of two or more objects

DOC: Medical Management Goals

Full participation in therapeutic activity

and daily routine – as possible

Prevent medical complications – skin

integrity, contractures, respiratory status

(sleep apnea, aspiration), bowel/bladder

maintenance

Stimulate (environmental,

pharmacologic)

DOC: Medical

Management

Also called

Dysautonomia

Sympathetic Storming

Autonomic Dysreflexia

Paroxysmal Autonomic

Instability with Dystonia

Treatment:

Environmental Control (light/sound)

Pharmacology

(propranolol, gabapentin,

clonidine)

AUTONOMIC DYSFUNCTION

SYNDROME (ADS)

15-33% TBI

Dystonia, agitation,

tachycardia,

hyperthermia,

hypertension,

diaphoresis

Neurobehavioral

Assessment of

DOC

ACCURATE

DIAGNOSIS

TREATMENT

PLANNING

PROGNOSIS

CAREGIVER

EDUCATION

Behavior Response

4 Spontaneously3 To speech2 To pain1 No response

5 Oriented to time, person & place

4 Confuses3 Inappropriate words2 Incomprehensible sounds1 No response

6 Obeys commands5 Moves to localized pain4 Flex to withdraw from pain3 Abnormal flexion2 Abnormal extension1 No response

Glasgow Coma

Scale (GCS)

The GCS is a

neurobehavioral scale

which provides an objective

assessment of coma or

impaired consciousness

A score of 13 to 15 correlates

to mTBI

A score between 9 and 12

correlates to a moderate TBI

A score below 8 correlates to

severe TBI

Goal Setting: Considerations

Goal Type Considerations/Examples

Response Based Base the goal on the response types exhibited by the person (no response/ generalized

response / localized response)

If the person currently responds to auditory stimuli in a generalized way, the logical goal

progression would be to the localized response level

Tolerance for Stimuli

or Intervention

Base the goal on the level of tolerance exhibited by the person for a given intervention

(see signs of distress in the ADS section of this chapter)

If the person begins to exhibit signs of distress after a given intervention has been

administered for 5 minutes, a logical goal might be to progress tolerance to 10 minutes

Risk Management There are a number of interventions designed to reduce risk for physical complications

(see physical management section of this chapter)

Goals based on these interventions are very appropriate for persons with DOC

Caregiver

Development

Goals related to the education and training of caregivers within the person’s support

system are integral in ensuring person-centered care

Some examples might include training in the appropriate administration of sensory

stimulation, monitoring for signs of distress, and follow-through with physical

management interventions such as range of motion

Sensory Stimulation Modalities

Sensory Modality Intervention Examples

Visual (seeing) Mirror, familiar photographs, bubbles, scenery and setting changes

Auditory (hearing) Pre-recorded voices of family members and friends, favorite music, as well as

environmental noises

Olfactory (smelling) Fragrances such as shampoos, cologne or perfumes, spices, and environmental scents

Gustatory (tasting) Lemon swabs, cotton-tipped applicators dipped in any variety of flavors preferred by

the person; gustatory stimulation should be directed by speech pathology due to the

inherent aspiration risks

Proprioceptive /

Vestibular (moving)

This modality involves the movement of the body in space as well as the awareness of

the position and movement of body parts, and includes range of motion, hand-over-

hand assistance for motor tasks, position changes, and movement of the wheelchair

Tactile (touching) Preferred textures (e.g., favorite stuffed animal, clothing items, etc.), alternating

smooth and rough textures (e.g., corduroy, sandpaper, silk)

Sensory Stimulation Response Monitoring

No Response (NR)

No discernable reflexive or volitional response

Generalized Response (GR)

Non-purposeful and non-specific reflexive response

Localized Response (LR)

Localized response that is not reflexive (e.g., turn head toward auditory stimuli)

Train family members on how

they can contribute and

participate in the

stimulation/ regulation

protocols

Response Monitoring Caregiver Education

Complex Physical Management

to Include in Treatment

Range of motion

Orthotic use

Upright positioning

Bed positioning

Fatigue and Sleep

Disturbance

Be familiar with the types of instruments to measure fatigue

Learning

Objectives

Distinguish between excessive daytime

sleepiness (EDS) and fatigue

Describe physiological

changes which contribute to sleep disturbances after

TBI

Understand pharmacological and non-pharmacological approaches to sleep

disturbance

Gain an Understanding of the Coping

Hypothesis

Explain the role of pain, depression and anxiety on

sleep

FATIGUE

32-73% report

fatigue after

brain injury

Can be chronic

And impact all

Aspects of life

Fatigue is the awareness of

a decreased capacity for

physical and/or mental

activity due to an

imbalance in the

availability, utilization

and/or restoration of

resources needed to

perform activity

Fatigue

Types of

Fatigue

Physiologicalhormones,

neurotransmitters,

nueral connections

Direct result of

BI/dysfunction

Psychological

High proportion of

people with BI

experience

anxiety/depression

Primary Secondary

Psychological – state of wearinessrelated to reduced motivation, mental

activity, boredom that occurs under

chronic stress, anxiety, depression

Impact – all areas of life (home,

work, social, school.

May be associated with muscle

Weakness/other changes in

Perhpheral nervous system

Primary and Secondary Fatigue

Sleep Disturbance

Pain

Stress

Depression

Anxiety

Primary

Diffuse injury

brain centers

which control

arousal,

attention,

response:

RAS

Limbic system

Middle frontal

Basal ganglia

Secondary

The Coping Hypothesis

This hypothesis suggests that fatigue

may come from the compensatory

effort necessary to meet the

demands of everyday life due to

cognitive deficits including impaired

attention and speed of processing

Cognitive demand, over time, may

require a greater level of effort to

maintain performance, creating

stress and fatigue

Association between difficulty with attention and information processing and

fatigue levels – greater cognitive exertion to complete tasks

Measures of Fatigue

The Visual Analogue Scale for Fatigue (VAS-F)

Assesses fatigue and energy at a single point in time

The Fatigue Severity Scale (FSS)

Assesses the impact of fatigue on daily function using 7 point scale

The Barrow Neurological Institute Fatigue Scale (BNI Fatigue Scale)

Assesses the difficulty level of energy and alertness

The Global Fatigue Index (GFI)

Assesses four domains of fatigue-severity, distress, impact on activity and

timing of fatigue

The Causes of Fatigue Questionnaire (COF)

Assesses the extent to which physical and mental activities may cause

fatigue

Strategies to Improve Energy

Reducing work hours

Taking frequent breaks

Participating in physical

conditioning activities

Addressing pain, anxiety

and/or depression

Modifying the pace or

demands of the task

Reducing distractions

Managing information

overload

PHYSICAL COGNITIVE

Sleep

Disturbances PAIN

MELATONIN

NAP

Changes

in REM

sleep

30-80% individuals with TBI

Narcolepsy

Sleep apnea

Post-traumatic hypersomnia

Periodic limb movement disorder

Causes: daytime napping, pain,

depression, anxiety, disruption of

normal circadian rhythm/melatonin

synthesis

COMMON SLEEP DISORDERS

Narcolepsy

Characterized by repeated episodes

of naps or lapses into sleep of short

duration usually less than one hour

Sleep Apnea Syndromes

Characterized by repetitive episodes

of upper airway obstruction that occur

during sleep (Obstructive) or

characterized by the decreasing or

stopping of breaths during sleep

(Central)

Post-Traumatic Hypersomnia

Excessive sleepiness that occurs as a result of a traumatic event involving the central nervous system

Periodic Limb Movement Disorder

Characterized by periodic episodes of repetitive and highly stereotyped limb (usually leg)

movements that occur during sleep

Insomnia

Characterized by difficulty falling asleep, frequent awakenings with difficulty then falling back to

sleep (>30 minutes) and a feeling of daytime fatigue and/or difficulty getting through the day

Diagnosis and

Treatment

DIAGNOSTIC TOOLS

Epworth Sleepiness Scale

Pittsburgh Sleep Quality Index

Polysomnography

Multiple Sleep Latency Test

There are still unanswered

questions about fatigue and

sleep disturbances, and

further study of interventions is

needed

Q & A

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