ANATOMY AND PHYSIOLOGY

ANATOMY AND PHYSIOLOGY
General functions of the neurologic system include:
† Cognition,

emotion, and memory. † Sensation, perception, and the integration of sensoryperceptual experience. † Regulation of homeostasis, consciousness, temperature, BP, and other bodily processes.

There are two types of nerve cells: (1) neuroglia and (2) neurons

Neuroglia
Functions: a. act as supportive tissue, nourishing and protecting the neurons b. maintain homeostasis in the interstitial fluid around the neurons and account for about 50 percent of the central nervous system (CNS) volume c. have the ability to regenerate and respond to injury by filling spaces left by damaged neurons.

Nervous Tissue: Support Cells
Support cells in the CNS are grouped together as ´neurogliaµ Function: to support, insulate, and protect neurons

Nervous Tissue: Support Cells
Astrocytes
† Abundant,

star-shaped cells † Brace neurons † Form barrier between capillaries and neurons † Control the chemical environment of the brain

Nervous Tissue: Support Cells

Nervous Tissue: Support Cells
Microglia
† Spiderlike

phagocytes † Dispose of debris

Nervous Tissue: Support Cells

Nervous Tissue: Support Cells
Ependymal cells
cavities of the brain and spinal cord † Circulate cerebrospinal fluid
† Line

Nervous Tissue: Support Cells

Nervous Tissue: Support Cells
Oligodendrocytes
around nerve fibers in the central nervous system † Produce myelin sheaths
† Wrap

Nervous Tissue: Support Cells

Nervous Tissue: Support Cells
Satellite cells
† Protect

neuron cell bodies

Schwann cells
† Form

myelin sheath in the peripheral nervous system

Nervous Tissue: Support Cells

Figure 7.3e

Neurons
Functions:
a. have the ability to produce action potentials or impulses (excitability or irritability) and b. to transmit impulses (conductivity).

Nervous Tissue: Neurons

Nervous Tissue: Neurons
Neurons = nerve cells
† Cells

specialized to transmit messages † Major regions of neurons
Cell body³nucleus and metabolic center of the cell  Processes³fibers that extend from the cell body 

Nervous Tissue: Neurons
Cell body
† Nissl 

substance

Specialized rough endoplasmic reticulum

† Neurofibrils

Intermediate cytoskeleton  Maintains cell shape 

Nervous Tissue: Neurons
Cell body
† Nucleus † Large

nucleolus

Processes outside the cell body
† Dendrites³conduct

impulses toward the cell body † Axons³conduct impulses away from the cell body

Nervous Tissue: Neurons
Axons end in axonal terminals Axonal terminals contain vesicles with neurotransmitters Axonal terminals are separated from the next neuron by a gap
† Synaptic

cleft³gap between adjacent neurons † Synapse³junction between nerves

Nervous Tissue: Neurons
Myelin sheath³whitish, fatty material covering axons Schwann cells³produce myelin sheaths in jelly roll² like fashion Nodes of Ranvier³gaps in myelin sheath along the axon

Neuron Cell Body Location
Most neuron cell bodies are found in the central nervous system
† Gray

matter³cell bodies and unmyelinated fibers † Nuclei³clusters of cell bodies within the white matter of the central nervous system

Ganglia³collections of cell bodies outside the central nervous system

Functional Classification of Neurons
Sensory (afferent) neurons
† Carry 

impulses from the sensory receptors to the CNS

Cutaneous sense organs  Proprioceptors³detect stretch or tension

Motor (efferent) neurons
† Carry

impulses from the central nervous system to viscera, muscles, or glands

Functional Classification of Neurons
Interneurons (association neurons)
† Found

in neural pathways in the central nervous system † Connect sensory and motor neurons

Neuron Classification

Structural Classification of Neurons
Multipolar neurons³many extensions from the cell body

Structural Classification of Neurons
Bipolar neurons³one axon and one dendrite

Structural Classification of Neurons
Unipolar neurons³have a short single process leaving the cell body

Figure 7.8c

Functional Properties of Neurons
Irritability
† Ability

to respond to stimuli to transmit an impulse

Conductivity
† Ability

Nerve Impulses
Resting neuron
The plasma membrane at rest is polarized † Fewer positive ions are inside the cell than outside the cell
†

Depolarization
A stimulus depolarizes the neuron·s membrane † A depolarized membrane allows sodium (Na+) to flow inside the membrane
†

The exchange of ions initiates an action potential in the neuron

Nerve Impulses
Action potential
the action potential (nerve impulse) starts, it is propagated over the entire axon † Impulses travel faster when fibers have a myelin sheath
† If

Nerve Impulses
Repolarization
† Potassium

ions rush out of the neuron after sodium ions rush in, which repolarizes the membrane † The sodium-potassium pump, using ATP, restores the original configuration

Transmission of a Signal at Synapses
Impulses are able to cross the synapse to another nerve
† Neurotransmitter

is released from a nerve·s axon

terminal † The dendrite of the next neuron has receptors that are stimulated by the neurotransmitter † An action potential is started in the dendrite

Transmission of a Signal at Synapses
Axon of transmitting neuron Axon terminal Vesicles Synaptic cleft Receiving neuron Action potential arrives

Synapse

Transmission of a Signal at Synapses
Axon of transmitting neuron Axon terminal Vesicles Synaptic cleft Receiving neuron Synapse Action potential arrives

Transmitting neuron Vesicle fuses with plasma membrane Synaptic cleft Ion channels

Receiving neuron

Transmission of a Signal at Synapses
Axon of transmitting neuron Axon terminal Vesicles Synaptic cleft Receiving neuron Synapse Action potential arrives

Transmitting neuron Vesicle fuses with plasma membrane Synaptic cleft Ion channels

Neurotransmitter is released into synaptic cleft Neurotransmitter molecules Receiving neuron

Transmission of a Signal at Synapses
Axon of transmitting neuron Axon terminal Vesicles Synaptic cleft Receiving neuron Synapse Action potential arrives

Transmitting neuron Vesicle fuses with plasma membrane Synaptic cleft Ion channels

Neurotransmitter is released into synaptic cleft Neurotransmitter molecules Receiving neuron

Neurotransmitter binds to receptor on receiving neuron¶s membrane

Transmission of a Signal at Synapses
Axon of transmitting neuron Axon terminal Vesicles Synaptic cleft Receiving neuron Synapse Action potential arrives

Transmitting neuron Vesicle fuses with plasma membrane Synaptic cleft Ion channels Neurotransmitter Receptor

Neurotransmitter is released into synaptic cleft Neurotransmitter molecules Receiving neuron

Neurotransmitter binds to receptor on receiving neuron¶s membrane

Na+

Ion channel opens

Transmission of a Signal at Synapses
Axon of transmitting neuron Axon terminal Vesicles Synaptic cleft Receiving neuron Synapse Action potential arrives

Transmitting neuron Vesicle fuses with plasma membrane Synaptic cleft Ion channels Neurotransmitter Receptor

Neurotransmitter is released into synaptic cleft Neurotransmitter molecules Receiving neuron

Neurotransmitter binds to receptor on receiving neuron¶s membrane

Neurotransmitter broken down and released Na+

Na+

Ion channel opens

Ion channel closes

Neurons band together into - peripheral nerves, - spinal nerves, - spinal cord, and - tissues of the brain.
These structures make up the neurologic system, which is divided into - the CNS and - the peripheral nervous system (PNS).

CENTRAL NERVOUS SYSTEM

consists of the:
brain spinal cord

Regions of the Brain: Cerebrum

Regions of the Brain: Cerebrum
Cerebral Hemispheres (Cerebrum)
† Paired

(left and right) superior parts of the brain † Includes more than half of the brain mass † The surface is made of ridges (gyri) and grooves (sulci)

Regions of the Brain: Cerebrum

Regions of the Brain: Cerebrum
Lobes of the cerebrum
† Fissures

(deep grooves) divide the cerebrum into lobes † Surface lobes of the cerebrum
Frontal lobe  Parietal lobe  Occipital lobe  Temporal lobe 

Regions of the Brain: Cerebrum

Regions of the Brain: Cerebrum
Specialized areas of the cerebrum
†

Primary somatic sensory area
Receives impulses from the body·s sensory receptors  Located in parietal lobe 

†

Primary motor area
Sends impulses to skeletal muscles  Located in frontal lobe 

†

Broca·s area 

Involved in our ability to speak

Regions of the Brain: Cerebrum

Regions of the Brain: Cerebrum

Figure 7.14

Regions of the Brain: Cerebrum
Cerebral areas involved in special senses
† Gustatory

area (taste) † Visual area † Auditory area † Olfactory area

Regions of the Brain: Cerebrum
Interpretation areas of the cerebrum
† Speech/language

region † Language comprehension region † General interpretation area

Regions of the Brain: Cerebrum
Layers of the cerebrum
† Gray

matter³outer layer in the cerebral cortex composed mostly of neuron cell bodies † White matter³fiber tracts deep to the gray matter 

Corpus callosum connects hemispheres

Basal nuclei³islands of gray matter buried within the white matter

Regions of the Brain: Cerebrum

Regions of the Brain: Diencephalon

Regions of the Brain: Diencephalon

Regions of the Brain: Diencephalon
Sits on top of the brain stem Enclosed by the cerebral hemispheres Made of three parts
† Thalamus † Hypothalamus † Epithalamus

Regions of the Brain: Diencephalon
The Diencephalon is the seat of the control system for impulse transmission to different parts of the brain

Regions of the Brain: Diencephalon
Thalamus
† Surrounds

the third ventricle † The relay station for sensory impulses † Transfers impulses to the correct part of the cortex for localization and interpretation

Regions of the Brain: Diencephalon
Hypothalamus
† Under

the thalamus † Important autonomic nervous system center
Helps regulate body temperature  Controls water balance  Regulates metabolism 

Regions of the Brain: Diencephalon
Hypothalamus (continued)
† An

important part of the limbic system (emotions) † The pituitary gland is attached to the hypothalamus

Regions of the Brain: Diencephalon
Epithalamus
† Forms

the roof of the third ventricle † Houses the pineal body (an endocrine gland) † Includes the choroid plexus³forms cerebrospinal fluid

Regions of the Brain: Brain Stem
Attaches to the spinal cord Parts of the brain stem
† Midbrain † Pons † Medulla

oblongata

Regions of the Brain: Brain Stem

Regions of the Brain: Brain Stem
Midbrain
† Mostly

composed of tracts of nerve fibers † Has two bulging fiber tracts³ cerebral peduncles † Has four rounded protrusions³ corpora quadrigemina 

Reflex centers for vision and hearing

Regions of the Brain: Brain Stem
Pons
bulging center part of the brain stem † Mostly composed of fiber tracts † Includes nuclei involved in the control of breathing
† The

Regions of the Brain: Brain Stem
Medulla Oblongata
The lowest part of the brain stem † Merges into the spinal cord † Includes important fiber tracts † Contains important control centers
† 
   

Heart rate control Blood pressure regulation Breathing Swallowing Vomiting

Regions of the Brain: Brain Stem
Reticular Formation
† Diffuse

mass of gray matter along the brain stem † Involved in motor control of visceral organs † Reticular activating system (RAS) plays a role in awake/sleep cycles and consciousness

Regions of the Brain: Cerebellum

Regions of the Brain: Cerebellum
Two hemispheres with convoluted surfaces Provides involuntary coordination of body movements

Protection of the Central Nervous System
Scalp and skin Skull and vertebral column Meninges Cerebrospinal fluid (CSF) Blood-brain barrier

Protection of the Central Nervous System

Meninges
Dura mater
† Double-layered 

external covering

Periosteum³attached to inner surface of the skull  Meningeal layer³outer covering of the brain
† Folds

inward in several areas

Meninges
Arachnoid layer
† Middle

layer † Web-like

Pia mater
layer † Clings to the surface of the brain
† Internal

Meninges

Cerebrospinal Fluid (CSF)
Similar to blood plasma composition Formed by the choroid plexus Forms a watery cushion to protect the brain Circulated in arachnoid space, ventricles, and central canal of the spinal cord

Ventricles and Location of the Cerebrospinal Fluid

Ventricles and Location of the Cerebrospinal Fluid

Blood-Brain Barrier
Includes the least permeable capillaries of the body Excludes many potentially harmful substances Useless as a barrier against some substances
Fats and fat soluble molecules † Respiratory gases † Alcohol † Nicotine † Anesthesia
†

Spinal Cord Anatomy

Spinal Cord Anatomy

Spinal Cord Anatomy
Internal gray matter is mostly cell bodies
† Dorsal

(posterior) horns † Anterior (ventral) horns † Gray matter surrounds the central canal 

Central canal is filled with cerebrospinal fluid

Exterior white mater³conduction tracts
† Dorsal,

lateral, ventral columns

Spinal Cord Anatomy
Meninges cover the spinal cord Spinal nerves leave at the level of each vertebrae
† Dorsal 

root

Associated with the dorsal root ganglia³collections of cell bodies outside the central nervous system

† Ventral 

root

Contains axons

Spinal Cord Anatomy

Spinal and Peripheral Nerves
Branching from the spinal cord are 31 pairs of spinal nerves: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal The spinal nerves contain both ascending and descending fibers, and although there is some overlap,each is responsible for innervation of a particular area of the body.

Dermatomes - are regions of the body innervated by the cutaneous branch of a single spinal nerve.

Pathways Between Brain and Spinal Cord

The Reflex Arc
Reflex³rapid, predictable, and involuntary response to a stimulus
† Occurs

over pathways called reflex arcs

Reflex arc³direct route from a sensory neuron, to an interneuron, to an effector

The Reflex Arc
Stimulus at distal end of neuron Receptor (a) Skin Sensory neuron Motor neuron Effector Spinal cord (in cross section) Integration center Interneuron

The Reflex Arc
Stimulus at distal end of neuron Receptor (a) Skin

The Reflex Arc
Stimulus at distal end of neuron Receptor (a) Skin Sensory neuron

The Reflex Arc
Stimulus at distal end of neuron Receptor (a) Skin Sensory neuron Spinal cord (in cross section) Integration center Interneuron

The Reflex Arc
Stimulus at distal end of neuron Receptor (a) Skin Sensory neuron Motor neuron Spinal cord (in cross section) Integration center Interneuron

The Reflex Arc
Stimulus at distal end of neuron Receptor (a) Skin Sensory neuron Motor neuron Effector Spinal cord (in cross section) Integration center Interneuron

Simple Reflex Arc
Sensory receptors (stretch receptors in the quadriceps muscle) Sensory (afferent) neuron Spinal cord Sensory receptors (pain receptors in the skin) Sensory (afferent) neuron Interneuron Motor (efferent) neuron Effector (biceps brachii (c) muscle)

Synapse in ventral horn gray matter

Motor (efferent) neuron

(b)

Effector (quadriceps muscle of thigh)

Simple Reflex Arc
Sensory receptors (stretch receptors in the quadriceps muscle) Spinal cord

(b)

Simple Reflex Arc
Sensory receptors (stretch receptors in the quadriceps muscle) Sensory (afferent) neuron Spinal cord

(b)

Simple Reflex Arc
Sensory receptors (stretch receptors in the quadriceps muscle) Sensory (afferent) neuron Spinal cord

Synapse in ventral horn gray matter

(b)

Simple Reflex Arc
Sensory receptors (stretch receptors in the quadriceps muscle) Sensory (afferent) neuron Spinal cord

Synapse in ventral horn gray matter

Motor (efferent) neuron

(b)

Simple Reflex Arc
Sensory receptors (stretch receptors in the quadriceps muscle) Sensory (afferent) neuron Spinal cord

Synapse in ventral horn gray matter

Motor (efferent) neuron

(b)

Effector (quadriceps muscle of thigh)

Simple Reflex Arc
Spinal cord Sensory receptors (pain receptors in the skin)

(c)

Simple Reflex Arc
Spinal cord Sensory receptors (pain receptors in the skin) Sensory (afferent) neuron

(c)

Simple Reflex Arc
Spinal cord Sensory receptors (pain receptors in the skin) Sensory (afferent) neuron Interneuron

(c)

Simple Reflex Arc
Spinal cord Sensory receptors (pain receptors in the skin) Sensory (afferent) neuron Interneuron Motor (efferent) neuron

(c)

Simple Reflex Arc
Spinal cord Sensory receptors (pain receptors in the skin) Sensory (afferent) neuron Interneuron Motor (efferent) neuron Effector (biceps brachii (c) muscle)

Types of Reflexes and Regulation
Somatic reflexes
† Activation

of skeletal muscles † Example: When you move your hand away from a hot stove

Types of Reflexes and Regulation
Autonomic reflexes
† Smooth

muscle regulation † Heart and blood pressure regulation † Regulation of glands † Digestive system regulation

Peripheral Nervous System (PNS)
Nerves and ganglia outside the central nervous system Nerve = bundle of neuron fibers Neuron fibers are bundled by connective tissue

PNS: Structure of a Nerve
Endoneurium surrounds each fiber Groups of fibers are bound into fascicles by perineurium Fascicles are bound together by epineurium

PNS: Structure of a Nerve

PNS: Classification of Nerves
Mixed nerves
† Both

sensory and motor fibers impulses toward the CNS impulses away from the CNS

Sensory (afferent) nerves
† Carry

Motor (efferent) nerves
† Carry

PNS: Cranial Nerves
12 pairs of nerves that mostly serve the head and neck Only the pair of vagus nerves extend to thoracic and abdominal cavities Most are mixed nerves, but three are sensory only

Cranial Nerves

PNS: The Cranial Nerves

PNS: The Cranial Nerves

PNS: The Cranial Nerves

PNS: The Cranial Nerves

NEUROLOGIC ASSESSMENT
By: Kirk Odrey O. Jimenez

Learning Objectives: After the presentation, we should be able to:
Perform a physical assessment of the neurologic system † Document neurologic system findings † Differentiate between normal and abnormal findings
†

INTRODUCTION
The human nervous system is a unique system that allows the body to interact with the environment as well as to maintain the activities of internal organs. The nervous system acts as the main ´circuit boardµ for every body system. Because the nervous system works so closely with every other system, a problem within another system or within the nervous system itself can cause the nervous system to ´short-circuit.µ (Dillon,2007)

A major goal of nursing is early detection to prevent or slow the progression of disease. So it is important for nurses to accurately perform a thorough neurologic assessment and to understand the implications of subtle changes in assessment findings. By doing so, we can initiate timely interventions that can save lives.
(Dillon,2007)

COMPONENTS OF NEUROLOGIC EXAM 

Mental Status
† † † † † † 

Sensory Function
† † † † † † † † †

a. Appearance/ Hygiene/ Grooming/ Odor b. Behavior c. Speech/ Communication d. Level of Consciousness e. Memory f. Cognitive function 

Cranial Nerve Function
(12 cranial nerves)

a. Light touch b. Pain c. Vibration d. Kinesthetics e. Streognosis f. Graphesthesia g. Two-point discrimination h. point localization i. Sensory Extinction a. Deep tendon reflexes b. Superficial reflexes 

Reflex Function 

Ensure proper hygiene before seeing a client Ensure all equipment is properly cleaned
Equipment Needed:
- BP cuff (128 or 256 Hz) - Penlight gloves - Wisp of cotton - Reflex hammer - Tuning fork - Nonsterile - Tongue blade 

- 

Sharp object such as toothpick or sterile needle Objects to touch: coin, button, key or paperclip Something fragrant: rubbing alcohol or coffee Something to taste: such as lemon juice, sugar or salt Two taste tubes or other vials Ophthalmoscope

Introduce self to the client.

Assessing the Mental Status
1. APPEARANCE/ HYGIENE/ GROOMING/ ODOR
a.

b.

Begin the assessment as the patient approaches you. Observe the general appearance, hygiene, grooming and the odor of the client.

Normal: 
  

good grooming, dress in appropriate to temperature & weather, no offensive or unpleasant odor hair well kept or tied

Abnormal:  Poor hygiene  Unpleasant or offensive body odor

2. BEHAVIOR a. Assess the client·s mood and emotions b. Observe body language and facial expression or affect c. Note his or her posture

Normal: 

Abnormal:   

Verbal expressions match with the nonverbal behavior Mood is appropriate to the situation Standing in upright stance with parallel alignment of hips &shoulders

Lack of facial expression
†

- Possible psychological disorder (e.g., depression or schizophrenia) or neurologic impairment affecting cranial nerves. - Parkinson·s disease. - Depression if psychological in origin; or stroke with hemiparesis if physiological in origin. 

Masklike expression:
† 

Slumped posture:
†

3. SPEECH/ COMMUNICATION a. Speech and Language 

Listen to patient·s rate and ease of speech, including enunciation. Show patient a picture and have him or her sees. Have patient repeat, ´do, ray, me, fa, so, la, ti, describe what he or she do.µ

b. Spontaneous Speech & Motor Speech 


c. Autonomic Speech 

Have patient say something that is committed to memory, such as days of week or months of year.

Normal:  Speech flows easily; patient enunciates clearly.  Sophistication of speech matches age, education, and fluency.

Abnormal:
Hesitancy, stuttering, stammering, unclear speech:
†

- Lack of familiarity with language, deference or shyness, anxiety, neurologic disorder. - Neurologic problems such as stroke. 

Dysphasia/aphasia:
†

Drugs and alcohol can also cause slurred speech.

Normal: 

Abnormal:  

Spontaneous speech intact. Motor speech intact.

Impaired spontaneous speech:
†

Cognitive impairment. 

Impaired motor speech (dysarthria):
†

Problem with CN XII

Normal:

Abnormal:

Automatic speech intact.

Impaired automatic speech:
† Cognitive

impairment

or memory

problem.

4. LEVEL OF CONSCIOUSNESS
a. Test orientation to time, place, and person

Normal: 

Abnormal: 
 

Awake, alert, and oriented to time, place, and person (AAO x 3) Responds to external stimuli 

  

Disorientation may be physical in origin Disorientation can also be psychiatric in origin (schizophrenia) Lathargic or somnolent Obtunded Stupor Coma

Glasgow Coma Scale
-

-

A standardized objective assessment that defines the LOC by giving it a numeric value. Most often after brain surgery Document as E_V_M_; for example, E4V5M6.

GLASGOW COMA SCALE
Eyes open E Spontaneously . . . . . . . . 4 To command . . . . . . . . . . 3 To pain . . . . . . . . . . . . . . . 2 Unresponsive. .. . . . . . . . . 1 Oriented . . . . . . . . . . . . . . . 5 Confused . . . . . . . . . . . . . . . 4 Inappropriate . . . . . . . . . . . . 3 Incomprehensible . . . . . . . . 2 Unresponsive. . . . . . . . . .. . . 1 Obeys commands . . . . . . . .. 6 Localizes pain. . . . . . . . . . . 5 Withdraws from pain. . . . «. 4 Abnormal flexion . . . . . . .. . . 3 Abnormal extension . . . . . . . 2 Unresponsive. . . . . . . . . . . . . 1 Findings

Best verbal response V

Findings

Best motor response M

Findings

Total______

From Wijdicks, et al, 2005, with permission.

The three numbers are added; the total score reflects the brain functional level. A fully awake person = 15 Coma = 7 or less The GCS assesses the functional state of the brain as a whole, not of any particular site in the brain. (Juarez and Lyon,1995)

Four Score Coma Measurement Scale
EYE RESPONSE 4 3 2 1 0 MOTOR RESPONSE 4 3 2 1 0 BRAINSTEM REFLEXES 4 3 2 1 0 RESPIRATION 4 3 2 1 0 Eyelids Eyelids Eyelids Eyelids Eyelids open or opened, tracking or blinking to command open but not tracking closed but open to loud voice closed but open to pain remain closed with pain

Thumbs up, fist, or peace sign to command Localizing to pain Flexion response to pain Extensor posturing No response to pain or generalized myoclonus status epilepticus

Pupil and corneal reflexes present One pupil wide and fixed Pupil or corneal reflexes absent Pupil and corneal reflexes absent Absent pupil, corneal, and cough reflex Not intubated, regular breathing pattern Not intubated, Cheyne-Stokes breathing pattern Not intubated, irregular breathing pattern Breathes above ventilator rate Breathes at ventilator rate or apnea

5. MEMORY
a. Test immediate recall: 

Ask patient to repeat three numbers, such as ´4, 9, 1.µ If patient can do so, ask her or him to repeat a series of five digits. Ask what patient had for breakfast. Ask patient to state his or her birthplace, recite his or her Social Security number, or identify a culturally specific person or event, such as the name of the previous president of the United States or the location of a natural disaster.

b. Test recent memory: 

c. Test long-term memory: 

Normal: Immediate, recent, and remote memory intact.

Abnormal: 

Memory problems can be benign or signal a more serious neurologic problem
†

such as Alzheimer·s disease. 

Forgetfulness - especially for immediate and recent events
†

often in older adults. 

With benign forgetfulness, person can retrace or use memory aids to help with recall.

Abnormal: 

Pathological memory loss
as inAlzheimer·s disease 

Temporary memory loss
may occur after head trauma. 

Retrograde amnesia
for events just preceding illness or injury. 

Postconcussion syndrome
can occur 2 weeks to 2 months after injury and may cause shortterm memory deficits.

6. COGNITIVE FUNCTION

a. Mathematical and Calculative Ability
† Ask

patient to perform a simple calculation, such as adding 4 x 4. If successful, proceed to more difficult calculation, such as 11/ 9.

Normal:
Mathematical/calcula tive ability intact and appropriate for patient·s age, educational level, and language facility.

Abnormal:
Inability to calculate at level appropriate to age, education, and language ability requires evaluation for neurologic impairment.

b. General Knowledge and Vocabulary
†

Ask how many days in a week and months in a year.

c. Thought Process
† † †

Ask patient to define familiar words such as ´apple,µ ´earthquake,µ and ´chastise.µ Begin with easy words and proceed to more difficult ones. Remember to consider the patient·s age, educational level, and cultural background.

Normal:

Abnormal:
Incoherent speech 
 

Thought process intact

illogical or unrealistic ideas repetition of words and phrases repeatedly straying from topic

suddenly losing train of thought (examples of altered thought processes that indicate need for further evaluation) Inability to define familiar words - requires further evaluation

d. Abstract Thinking
† Assess

the client to think abstractly. † Quote a proverb and ask the client to explain it·s meaning

Normal: 

Abnormal: 

Able to generalize from specific example and apply statement to human behavior. Children should be able to distinguish like from unlike as appropriate for their age and language facility.

Impaired ability to think abstractly:
†

Dementia, delirium, mental retardation, psychoses.

e. Judgment
† Observe

patient·s response to current situation. † Ask patient to respond to a situation or hypothetical situation.

Normal:

Abnormal:

Judgment appropriate and intact.

Impaired judgment can be associated with dementia, psychosis, or drug and alcohol abuse.

Assessing the CRANIAL NERVES
CN I³Olfactory Nerve a. Before testing nerve function, ensure patency of each nostril by occluding in turn and asking patient to sniff. b. Once patency is established, ask patient to close eyes. c. Occlude one nostril and hold aromatic substance such as coffee beneath nose. d. Ask patient to identify substance. e. Repeat with other nostril.

Normal: Patient is able to identify substance. 

Abnormal:
Anosmia is loss of sense of smell.
†

(Bear in mind that some substances may be unfamiliar, especially to children.)

†

†

May be inherited and nonpathological: chronic rhinitis, sinusitis, heavy smoking, zinc deficiency, or cocaine use. It may also indicate cranial nerve damage from facial fractures or head injuries, disorders of base of frontal lobe such as a tumor, or artherosclerotic changes. Persons with anosmia usually also have taste problems.

2. CNs II, III, IV, and VI³Optic, Oculomotor, Trochlear, and Abducens Nerves
Ask the client to read a printed material, observe the distance between the printed material and the client·s eyes. Use the snellen chart to check/ test:
distant vision Color

Client should be 20 feet distant from the chart Use an object to occlude one eye Evaluate the vision one eye at a time

c.

Evaluate the Extra Ocular Movements of the Eyes Convergens & Accomodation Pupillary Light Reflex

d.

e.

Testing eye movements

‡

- using direct and consensual pupillary reaction to light

Testing pupil accommodation

Normal:
Able to read without difficulty Visual acuity intact 20/20, both eyes 

Abnormal:
CN II deficits
†

can occur with stroke or brain tumor. can signal CN III deficits.

Changes in pupillary reactions
†

Hippus phenomenon: - Brisk constriction of pupils in reaction to light, followed by dilation and constriction

-may be normal or sign of early CN III compression.

Increased ICP causes changes in pupillary reaction. As pressure increases, response becomes more sluggish until pupils finally become fixed and dilated.

3. CN V³Trigeminal Nerve

a. Testing motor function:
Ask patient to move jaw from side to side against resistance and then clench jaw as you palpate contraction of temporal and masseter muscles, or to bite down on a tongue blade.

Testing CN V ² motor function

b. Testing sensory function: Ask patient to close eyes Touch the face with the wisp of cotton Instruct to tell you when he or she feels sensation on the face. Repeat the test using sharp and dull stimuli (toothpick) Instruct to say ´Sharpµ or ´Dullµ
(Be random, don·t establish a pattern)

Testing CN V ² sensory function

Compare both bilaterally.

c. Testing corneal reflex:
‡ ‡

Gently touch cornea with cotton wisp. Touching cornea can cause abrasions. Alternative approach is to: 
>

puff air across cornea with a needless syringe, or gently touch eyelash and look for blink reflex.

Testing corneal reflex

Normal: 

Abnormal:
Weak or absent contraction unilaterally:
† 

Full range of motion (ROM) in jaw and 15 strength. Patient perceives light touch and superficial pain bilaterally.

- Lesion of nerve, cervical spine, or brainstem.

Inability to perceive light touch and superficial pain
†

- may indicate peripheral nerve damage. - Neuralgic pain of CN V caused by the pressure of degeneration of a nerve.

Tic douloureux:
†

Corneal reflex test used in patients with decreased LOC
†

- to evaluate integrity of brainstem.

4. CN VII³Facial Nerve

Testing motor function:
Ask patient to perform these movements: smile, frown, raise eyebrows, show upper teeth, show lower teeth, puff out cheeks, purse lips, close eyes tightly while nurse tries to open them.
Testing CN VII ² motor function

b. Testing sensory function: - Test taste on anterior two-thirds of tongue for sweet, sour, salty. Sweet: Tip of the tongue Bitter: Back of tongue Sour: Sides of back half of tongue Salty: Anterior sides and tip of tongue

Testing taste sensation

Normal:  Facial nerve intact; able to make faces.  Taste sensation on anterior tongue intact.
†

Abnormal:
Asymmetrical or impaired movement:
†

Nerve damage, such as that caused by Bell·s palsy or stroke. Damage to facial nerve, chemotherapy or radiation therapy to head and neck.

Impaired taste/loss of taste:
†

(Taste decreased in older adults.)

5.

CN VIII³Acoustic Nerve
a. Perform Weber and Rinne tests for hearing b. Perform watch-tick test by holding watch close to patient·s ear. c. Perform Romberg test for balance Nurse at the back or side of the pt. Instruct client to stand straight, feet together, hands at the side and eyes closed.
‡

Watch tick test

(Evaluates the balancing function of the CN VIII)

Normal: 


Abnormal: 

Hearing intact. Negative Romberg test.

Hearing loss, nystagmus, balance disturbance, dizziness/vertigo:
†

Acoustic nerve damage. CN VIII, brainstem, or cerebellum problem or phenytoin (Dilantin) toxicity. 

Nystagmus:
†

6. CNs IX and X³Glossopharyngeal and Vagus Nerves a. Observe ability to cough, swallow, and talk. b. Test motor function:

Ask patient to open mouth and say ´ahµ while you depress Testing CN IX the tongue with a tongue blade. and X ² motor Observe soft palate and uvula. Soft palate and uvula should function rise medially.

c. Test sensory function of CN IX and motor function of CN X by stimulating gag reflex.
Tell patient that you are going to touch interior throat then lightly touch tip of tongue blade to posterior pharyngeal wall. Observe the pharyngeal movement. Ask the client to drink a small amount of water 


Testing CN IX and X ² motor function

Note the ease & difficulty of swallowing Note quality of the voice or hoarseness when speaking

Normal: 

Abnormal:
Unilateral movement:
† 



Swallow and cough reflex intact. Speech clear. Elevation and constriction of pharyngeal musculature and tongue retraction indicate positive gag reflex.

-Contralateral nerve damage.

†

Damage to CNs IX and X also impairs swallowing.

Changes in voice quality (e.g., hoarseness): CN X damage.
†

-CN X damage may also affect vital functions, causing arrhythmias because vagus nerve innervates most of viscera through parasympathetic system. Evaluate further because patient is at increased risk for aspiration.

Diminished/absent gag reflex: Nerve damage.
†

Impaired taste on posterior portion of tongue:
Problem with CN IX.

7. CN XI³Accessory Nerve

Test motor function of shoulder and neck muscles:
Ask patient to shrug shoulders upward against your resistance. (Trapieze muscle) Then ask her or him to turn head from side to side against your resistance.
(Strenoclaidomastoid msucle)

Observe for symmetry of contraction and muscle strength.

Normal:  Movement symmetrical, with patient moving against resistance without pain.  Full ROM of neck with +5/5 strength.

Abnormal: 
   

Asymmetrical Diminished Absent movement Pain unilateral or bilateral weakness:
†

Peripheral nerve CN XI damage.

8. CN XII³Hypoglossal Nerve

a. Have patient say ´d, l, n, tµ or a phrase

containing these letters.
The ability to say these letters requires use of the tongue.

b. Ask the patient to protrude the tongue.
Observe any deviation from midline, tumors, lesions, or atrophy. Now ask the patient to move the tongue from side to side.

Testing CN XII ² motor function

Normal: 

Abnormal:
Asymmetrical/diminished/ absent movement/deviation from midline/protruded tongue:
† 

Can protrude tongue medially. No atrophy, tumors, or lesions.

- Peripheral nerve CN XII damage.

Tongue paralysis results in dysarthria.

Assessing Sensory Function
1. Light Touch
Brush a light stimulus such as a cotton wisp over patient·s skin in several locations, including torso and extremities.

Normal:

Abnormal:
Diminished/absent cutaneous perception:
†

Identifies areas stimulated by light touch.

Peripheral nerve damage or damage to posterior column of spinal cord.

Peripheral neuropathies can also cause sensory deficits.
† † †

Hypesthesia: Increased sensitivity. Paresthesia: Numbness and tingling. Anesthesia: Loss of sensation.

2 . Pain
Stimulate skin lightly with sharp and dull ends of toothpick/ paper clip Apply stimuli randomly and ask patient to identify whether sensation is sharp or dull.

Touch patient·s skin with test tubes filled with hot or cold water. Apply stimuli randomly, and ask patient to identify whether sensation is hot or cold.

2

-

Normal:

Abnormal:
Diminished or absent pain perception:
†

Identifies areas stimulated and type of stimulation

Peripheral nerve damage or damage to lateral spinothalamic tract.

Hyperalgia: Increased pain sensation. Hypoalgesia: Decreased pain sensation. Analgesia: No pain sensation. Diminished/absent temperature perception:
†

Peripheral nerve damage or damage to lateral spinothalamic tract 

.

3. Vibration
Place a vibrating tuning fork over a finger joint, and then over a toe joint. Ask patient to tell you when vibration is felt and when it stops. If patient is unable to detect vibration, test proximal areas as well.

-

Normal:

Abnormal:

Vibratory sensation intact bilaterally in upper and lower extremities.

Diminished/absent vibration sense:
†

Peripheral nerve damage caused by alcoholism, diabetes, or damage to posterior column of spinal cord.

4. Kinesthetics (Position Sense)
Determine patient·s ability to perceive passive movement of extremities. Hold fingers on sides and move up and down, and have patient identify direction of movement. Flex and extend patient·s big toe, and ask patient to describe movement as up or down.

‡ Avoid moving the patient·s finger by placing your finger on top of the patient·s because the patient may sense the pressure of your finger rather than a true position change. ‡ If position sensation is intact distally, it is intact proximally.

Normal:

Abnormal:

Position sensation intact bilaterally in upper and lower extremities.

Diminished or absent position sense:
† Peripheral

nerve damage or damage to posterior column of spinal cord.

5. Stereognosis
With patient·s eyes closed, place a familiar object, such as a coin or a button, in patient·s hand, and ask patient to identify it.
Test both hands using different objects.

Normal:

Stereognosis intact bilaterally.

Abnormal: Abnormal findings suggest a lesion or other disorder involving sensory cortex or a disorder affecting posteriorcolumn.

6. Graphesthesia
With patient·s eyes closed, use point of a closed pen to trace a number on patient·s hand Ask patient to identify the number.

Normal:

Abnormal:

Graphesthesia intact bilaterally.

Abnormal findings suggest lesion or other disorder involving sensory cortex or disorder affecting posterior column.

7. Two-Point Discrimination
Ability to differentiate between two points of simultaneous stimulation.
Using ends of two toothpicks/ paper clip, stimulate two points on fingertips simultaneously. Gradually move toothpicks together, and assess smallest distance at which patient can still discriminate two points (minimal perceptible distance). Document distance and location.

Normal: Discriminates between two points on fingertips no more than 0.5 cm apart and on hands no more than 2 cm apart.

Abnormal:

Abnormal findings suggest lesion or other disorder involving sensory cortex or disorder affecting posterior column.

8. Point Localization Ability to sense and locate area being stimulated.
With patient·s eyes closed, touch an area; then have patient point to where he or she was touched. Test both sides and upper and lower extremities.

Normal:

Abnormal:

Point localization intact

Abnormal findings suggest lesion or other disorder involving sensory cortex or disorder affecting posterior column.

9. Sensory Extinction

.

Simultaneously touch both sides of patient·s body at same point. Ask patient to point to where she or he was touched.

Normal:

Extinction intact.

Abnormal: Identification of stimulus on only one side suggests lesion or other disorder involving sensory cortical region in opposite hemisphere.

REFLEXES
Documenting Reflex Findings Use these grading scales to rate the strength of each reflex in a deep tendon and superficial reflex assessment.

Deep tendon reflex grades 0 absent + present but diminished + + normal + + + increased but not necessarily pathologic + + + + hyperactive or clonic (involuntary contraction and relaxation of skeletal muscle) Superficial reflex grades 0 absent + present

Documentation of reflex finding

ASSESSING REFLEXES
1. Deep Tendon Reflexes a. Biceps Reflex Normal: Contraction of biceps with flexion of forearm. +2

Rest patient·s elbow in your non-dominant hand, with your thumb over biceps tendon. Strike your thumbnail.

b. Triceps Reflex
Abduct patient·s arm and flex it at the elbow. Support the arm with your nondominant hand. Strike triceps tendon about 1 to 2 inches above olecranon process, approaching it from directly behind.

Normal: Contraction of triceps with extension at elbow. +2

c. Patellar Reflex

Normal: Contraction of quadriceps with extension of knee. +2

Have patient sit with legs dangling. Strike tendon directly below patella..

d. Achilles Reflex

Normal:

Have patient lie supine or sit with one knee flexed. Holding patient·s foot slightly dorsiflexed, strike Achilles tendon. Then quickly but gently hit it with a hammer

Plantar flexion of foot. +2

e. Test for Ankle Clonus

If you get 4 reflexes (++++) while supporting leg and foot, quickly dorsiflex foot.

Normal:

No contraction

Abnormal: Absent/diminished DTRs: - Degenerative disease; damage to peripheral nerve such as peripheral neuropathy; lower motor neuron disorder, such as ALS and Guillain-Barré syndrome. Hyperactive reflexes with clonus: - Spinal cord injuries, upper motor neuron disease such as MS. Rhythmic contraction of leg muscles and foot is positive sign of clonus - indicates upper motor neuron disorder.

2. Superficial Reflexes
a. Abdominal Reflex

Normal: Contraction of rectus abdominis. Umbilicus moves toward stimulus. Anus puckers.

Stroke patient·s abdomen diagonally from upper and lower quadrants toward umbilicus. Gently stroke skin around anus with gloved finger.

b. Cremasteric Reflex

Normal: Testes rise.

Gently stroke inner aspect of a male·s thigh.

c. Bulbocavernosus Reflex

Normal: Bulbocavernosus muscle contracts.

Gently apply pressure over bulbocavernous muscle on dorsal side of penis.

d. Plantar Reflex (Babinski·s Response)

Normal:

Stroke sole of patient·s foot in an arc from lateral heel to medial ball.

Flexion of all toes.

Assessing the Cerebellar Function
1. Balance tests

.

a.

a. Gait
Observe as the person walks 10-20 feet, turns, and returns to the starting point.

Normal: 
  

Abnormal: 

Person moves with a sense of freedom. Gait is smooth, rhythmic, and effortless Opposing arm swing is coordinated The turns are smooth 

 

Stiff, immobile posture. Staggering or reeling. Wide base of support Lack of arm swing or rigid arms Unequal rhythm of steps. Slapping of foot. Scraping of toe of shoe Ataxia ² uncoordinated or unsteady gait.

Perform Tandem Walking ask the person to walk a straight line in a heel-to-toe fashion.
This decreases the base of support and will accentuate any problem with coordination.

Normal:

Abnormal: 


Person can walk straight and stay balanced  

Crooked line walk Widens base to maintain balance Staggering, reeling, loss of balance An ataxia that did not appear now. Inability to tandem walk is sensitive for an upper motor neuron lesion, such as multiple sclerosis.

shallow knee bend or hop test
Ask the person to perform a shallow knee bend or hop in place, first on one leg, then the other.
this demonstrates normal position sense, muscle strength, and cerebellar function.

(some individuals cannot hop owing to aging or obesity)

b. Romberg·s test Stay at the person·s side or back, allow the person to close her eyes. You may stay at the person·s sfront, lest the person stand erect with eye closed. Gently push the person at the at the forehead

Normal:

Abnormal:
Sways, falls, widens base of feet to avoid falling Positive Romberg sign † Loss of balance that occurs when closing the eyes. † Occurs with cerebellar ataxia (multiple sclerosis, alcohol intoxication) † Loss of proprioception, and loss of vestibular function

Negative Romberg test

2. Coordination and Skilled Movements
a. Rapid Alternating Movements (RAM)

Ask the person to pat the knees with both hands, lift up, turn hands over, and pat the knees with the backs of the hands. Then ask to do this faster.

Normal:

Abnormal:

done with equal turning and quick rhythmic pace

Lack of coordination Dysdiadochokinesia
Slow, clumsy, and sloppy response † occurs with cerebellar disease
†

b. Finger-to-Finger test With the persons eyes open, ask that he or she use index finger to touch your finger, then his or her own nose. After a few times move your finger to a different spot.

Normal:

Abnormal:
Dysmetria
† †

Movement is smooth and accurate

clumsy movement with overshooting the mark occurs with cerebellar disorder constant deviation to one side

Past-pointing
†

c. Finger-to-nose test

Ask the person to close the eyes and to stretch out the arms. Ask the person to touch the tip of his or her nose with each index finger, alternating hands and increasing speed.

Normal:

Abnormal:

Done with accurate and smooth movement

Misses nose. Worsening of coordination when the eyes are closed
†

occurs with cerebellar disease

DIAGNOSTIC TESTS

Diagnostic Procedure
Computed Tomography Scanning Visualize sections of the spinal cord as well as intracranial contents The injection of a water-soluble iodinated watercontrast into the subarachnoid space through lumbar puncture helps noninvasive and painless  has a high degree of sensitivity for detecting lesions. Use of xray beams cross section Use : to identify intracranial tumor, hemorrhage, cerebral atrophy, calcification, edema, infarction, congenital abnormality.

Nursing Interventions   

  

teaching the client about the need to lie quietly throughout the procedure. Relaxation technique maybe helpful for clients with claustrophobia. Assess for iodine/shellfish allergy. Secure patent IV line. NPO if with contrast medium, for 4 hrs. Monitor for allergic reaction: flushing, nausea and vomiting.

Magnetic Resonance Imaging

Diagnostic Procedure
Magnetic Resonance Imaging Uses a powerful magnetic field to obtain images of different areas of the body. Can be performed with or without a contrast agent and can identify a cerebral abnormality earlier and more clearly than other diagnostic tests. Useful in diagnosis of multiple sclerosis and can describe the activity and the extent of disease in the brain and spinal cord. Cerebral Angiography Is an x-ray study of the cerebral circulation with a xcontrast agent injected into a selected artery (femoral) Visualize aneurysm

Nursing Interventions 
Obtain

history of metal implants. Remove all metal implants.

objects. Inform the client that the procedure last for 30 to 90 mins. mins. Patient preparation should include teaching relaxation technique. Inform the client that a narrow, tunnel like machine will enclose him/her during the procedure. Sedation may be needed for claustrophobic client. Obtain a signed consent. Hydrate the client, clear liquids are usually permitted. Instruct the client to void before the procedure.

Cerebral Angiography

Diagnostic Procedure
Myelography Contrast agent are injected into spinal subarachnoid space to permit visualization of spinal cord. Shows any distortion of the spinal cord or spinal dural sac caused by tumors, cysts, herniated vertebral disks or other lesions.

Nursing Interventions 
Instruct

the patient to remain immobile during the

test. Tell the client to expect a brief feeling of warmth in the face, behind the eyes or in the jaw, teeth, tongue, and lips, and a metallic taste when the contrast is injected. After the procedure check LOC, and injection site should be observed. Explain the procedure. Obtain a signed consent. Withhold oral intake 4-6 hours before the test. 4After the procedure: For pantopaque myelogram (oil-based) pt lies flat for (oil6-24 hours.

Diagnostic Procedure
Electroencephalography Graphic record of the electrical activity generated in the brain. EEG is a useful test for diagnosing and evaluating seizure disorders, coma, or organic brain syndrome. A sleep EEG may be recorded after sedation because some abnormal brain waves are seen only when the patient is asleep.

Nursing Interventions
metrizamide myelogram (water-based), HOB is (waterelevated at 30 degrees for at least 8 hours. Encourage fluid intake Explain the procedure, assure the client he/she will not receive electrical shock. The nurse needs to check doctor s order regarding the administration of antiseizure medication prior to testing. Withhold tranquillizer and stimulants for 24 to 48 hours. Inform the client that the standard EEG takes 45 to 60 minutes and 12 hours for sleep EEG. 
For

Electroencephalography

Measurement of the electrical activity Of the brain done during: ‡Relax ‡Hyperventilate ‡Sleeping ‡Flickering lights

Lumbar puncture
‡Insertion of needle in the sub arachnoid space ‡Assess the csf

Lumbar Puncture
Lumbar Puncture  Is carried out by inserting a needle into the lumbar subarachnoid space to withdraw CSF for diagnostic or therapeutic purposes.  The needle is usually inserted between L4 and L5.
Maintain position, usually lateral horizontal with knees to chest, chin on chest.  Obtain signed consent.  Explain the procedure.  Observe for complication following the procedure.  Keeping the patient in prone position overnight may reduce the incidence of headache. 

Electromyography

Nursing Interventions 

Obtain

by inserting needle electrodes into the skeletal muscles. Measure changes in the electrical potential of the muscles and the nerves leading to them. Useful in determining neuromuscular disorders and myopathies. 

Explain

the procedure. The patient is warned to expect a sensation similar to that of an intramuscular injection and the muscle examined may ache for a short time after the procedure.

Electromyogram

Measure the action potential and electrical activities of peripheral nerves

Pneumoencephalography 
Special

Nursing Interventions
written consent. Sedate as ordered. GA may be used. Inform the client that the procedure takes 2 hours. Inform the client that he/she may experience discomfort, N/V, after the procedure. After the procedure keep the client flat in bed for 24 to 48 hours. Monitor VS and neurologic checks. 
Secure

contrast study of the ventricular and cisternal system using air as contrast medium. Permits accurate localization of brain lesions by spinal or cisternal puncture with x-ray xexamination.

sources
Dillon, Patricia. Nursing Health Assessment. 2nd Ed. F.A. Davis. 2007 Jarvis, Carolyn. Physical Examination and Health Assessment. 3rd ed. New York: W.B. Saunder Company.2000 Bickley. Lyn and Hoekenan, Robert. Bate·s Guide to Physical Examination and History Taking. 7th ed. New York: Lippincott Williams and Wilkins. 1999 Estes, Mary Ellen Zator. Health Assessment & Physical Examination. 3rd ed. Delmar Learning. 2006

COMMON HEALTH PROBLEMS OF THE YOUNG ADULT

Multiple Sclerosis
MS is:  chronic, degenerative disease of the central nervous system that is characterized by demyelination of the nerve fibers of the brain and spinal cord.  Gen. characterized by exacerbations and remisions (relapsing-remitting type0  Although the cause of MS is unknown, it appears to be related to autoimmune disorder and viral infections.  commonly appears during adulthood (ages 20 to 40). W>M  Areas of the CNS most commonly affected brainstem, cerebrum, cerebellum, optic nerves, and the spinal cord.

Process of Demylination

Pathophysiology
MS
Causes §Unknown §Viral infection §Autoimmune disease

Multiple foci of dmyelination in the white matter (brainstem, spinal cord, optic nerves, cerebrum) Then later the gray matter.

Destruction of the myelin sheath (SCHWANN¶S CELLS)

INTERRUPTION/DISTORTION OF IMPULSE (SLOWED/BLOCKED)

Assessment 


Sign and symptoms of MS is characterized by remissions and exacerbation of symptoms. Symptoms vary depending on the area of the CNS involved, but generally include: 
      

Visual disturbances (diplopia, partial or total loss of vision, nystagmus) Scanning speech (slow, monotonous, slurred) Tremors Weakness/numbness of the extremities Fatigue Increased susceptibility to URTI Dysphagia Ataxic gait

Diagnostic Test 

Lumbar Puncture-total CSF protein is normal; IgG (gamma
globulin is elevated- IgG reflects hyperactivity of the immune system due to chronic demyelinaton) 

  

EEG-abnormalities in brain waves CT scan/ MRI reveals multifocal white matter lesion Myelogram Skull x-ray

Nursing Diagnoses for MS:
† Risks:

Ineffective breathing pattern; airway clearance; impaired³swallowing, physical mobility, skin integrity; altered nutrition; urinary incontinence; constipation

Interventions for MS:
There is no specific treatment for MS. Treatment includes:  physical therapy- to assist with motor dysfunction, such as problem with balance, stregnth, and motor coordination.  speech therapy- to manage dysarthria  drug therapy  Glucocorticoids (Prednisone, Dexamethasone, Corticotropin)- to reduce edema of the myelin sheet; sppeds recovery from attack  Muscle relaxant (Baclofen)- to treat spasticity  Amantadine, Ritalin, or antidepressants ²to manage fatigue  Low-dose TCAs- to manage sensory symptoms such as pains, numbness, burning, and tingling sensationsAntihistamines with vision therapy & exercises to minimize vertigo

Nursing Responsibilities/ Considerations for MS: 
    

Provide regular activity, rest, and relaxation. Assist with physical therapy: muscle stretching, relaxation and coordination exercise, walking exercise. Encourage well balanced, high fiber diet. Force fluids to prevent constipation. Avoid hot baths. Provide skin care to prevent skin breakdown.

Nursing Responsibilities/ Considerations for MS cont.: 

Patient and family teaching to promote emotional stability
Help patient establish daily routine, and help family understand patient·s changes in personality and physical capabilities. Inform the pt that exacerbations are unpredictable, necessitating physical & emotional adjustments in lifestyle eye patch Speech therapy Medicate and watch for adverse effects

-

Evaluate
Respiration; nutrition; ADLs; skin; bowel elimination; urinary incontinence

Myasthenia Gravis
progressive neuromuscular disorder that results in the failure to transmit nerve impulses at the MYONEURAL JUNCTION causing extreme weakness 

Failure of transmission is due to decreased

acetylcholine 

Women

> Men; 3 times more common in women  Young adults 20-30  secretion and increased cholinesterase at the nerve ending. 

Autoimmune disease.
† Characterized

by progressive weakness and abnormal fatigability of the skeletal muscles. † Commonly affects muscles innervated by the cranial nerves (face, lips, tongue, neck, and throat) † Exacerbated by exercise & repetitive movement † Occurs along with thymic abnormalities in 75% of pts

Pathophysiology:
Transmission of nurve impulses at the neuromuscular junction FAILS. Antireceptor antibodies block, weaken, or reduce the number of acetylcholyne Ach receptors available at each neuromuscular juction,thereby impairing the muscle depolarization necessary for movement

Myasthenia Gravis
Cause: Autoimmune response leading to ineffective acetylcholine release and inadequate muscle fiber response to Ach. Complications:
Aspiration † Pneumonia † Respiratory distress
†

Assessment
S&S 


Skeletal muscle weakness, fatigue Weak eye closure,ptosis, diplopia,

Rationale/ Pathophysiologic Basis due to impaired neuromuscular transmission due to impaired neuromuscular transmission to the cranial nerves supplying the eye muscles Impaired transmission of the cranial nerves innervating the facial muscles Due to impaired neuromuscular transmission to the diaphragm due to loss of ACh receptors in the appropriate junctions 



´snarl smileµ (smiles slowly) Masklike facial expression; Impaired speech; drooling Weakened respiratory muscles
Muscle are usually strongest in the morning but become progressively weaker during the day and following an exercise. 

Myasthenia Gravis

Skeletal muscle weakness

Diagnostic Test 

Tensilon Test (Edrophonium Chloride Test)  Short acting cholinergic is administered.  Reveals Increased muscle strength is observed (+ Tensilon Test) within 30-60 secs after IV injectio of edrophonium (tensilon) or Neostigmine (Prostigmin), lasting up to 30 mins. Single fiber electromyography with neural stimulation at the specific muscle fiber- progressive decrease in muscle fiber contraction Chest x-ray- reveals thymoma in 15% of pts

Treatment of Myasthenia Gravis
Anticholinesterase drugs, such as neostigmine and pyridostigmine- to counteract fatigue and muscle weaknes and allow for about 80% of normal muscle
†

Anticholinesterase drugs are not effective during myasthenic crisis, so they are discontinued until respiratory function begins to improve

Plasmapheresis (Removing the plasma from the blood) Immunosuppresive therapy with corticosteroids, azathioprine (Imuran) ² to decrease the immune response toward Ach receptors at the neuromuscular junction IgG during acute relapses- to suppress the immune system Thymectomy- to remove thymomas Tracheostomy, suctioning to remove secretions

Nursing Goals and Interventions 
  

     

Establish neurologic and respiratory baselines Assess swallowing / gag reflex before feeding the client. Plan exercise, meals, patient care & activities to make the most of energy peaks. Ex.,administer medications 20-30 minutes before meal to facilitate chewing or swallowing. Start meal with cold beverage. Administer medication at precise time to prevent relapses. Protect the client from falls. Provide adequate ventilation. Avoid exposure to infection, stree, strenous exercise, and needless exposure to the sun r cold. Frequent rest periods. Be prepared to give atropine for anticholinesterase overdose or toxicity 

 

Aerosol, pesticides/cleaners should also be avoided, Avoid alcohol, tonic water, and cigarette smoke. Pharmacotherapy 

Cholinergics (Anticholinesterase) 
 

Neostigmine (Postigmin) Pyridostigmin (Mestinon) Ambenomium (Mytelase) 



Glucocorticoids Antacids

Client with Huntington·s Disease (chorea)
Progressive, degenerative inherited neurologic disease characterized by increasing dementia and chorea (rapid, jerky involuntary movements) Cause unknown No cure Usually asymptomatic until age of 30 ² 40

Pathophysiology
involves destruction of cells in basal ganglia and other brain areas, decrease in acetylcholine

Manifestations
Abnormal movement and progressive dementia Early signs are personality change with severe depression, memory loss; mood swings, signs of dementia Increasing restlessness, worsened by environmental stimuli and emotional stress; arms and face and entire body develops choreiform movements, lurching gait; difficulty swallowing, chewing, speaking Slow progressive debilitation and total dependence Death usually results from aspiration pneumonia or another infectious process

Collaborative Care
almost always requires long-term care

Diagnostic Tests
genetic testing of blood

Medications
Antipsychotic (phenothiazines and butyrophenones) to restore neurotransmitters Antidepressants

Nursing Care
Very challenging: physiological, psychosocial and ethical problems Genetic counseling

Nursing Diagnoses
Risk for Aspiration Imbalanced Nutrition: Less than body requirements Impaired Skin Integrity Impaired Verbal Communication

Home Care
Referral to agencies to assist client and family, support group and organization

Client with Amyotrophic Lateral Sclerosis (ALS)
Progressive, degenerative neurologic disease characterized by weakness and wasting of muscles without sensory or cognitive changes Several types of disease including a familial type; onset is usually between age of 40 ² 60; higher incidence in males at earlier ages but equally post menopause Physiologic problems involve swallowing, managing secretions, communication, respiratory muscle dysfunction Death usually occurs in 2 ² 5 years due to respiratory failure

Amyotrophic Lateral Sclerosis

Pathophysiology
Degeneration and demyelination of motor neurons in anterior horn of spinal cord, brain stem and cerebral cortex Involves upper and lower motor neurons Reinnervation occurs in the early course of disease, but fails as disease progresses

Manifestations
Initial: spastic, weak muscles with increased DTRs (UMN involvement); muscle flaccidity, paresis, paralysis, atrophy (LMN involvement); clients note muscle weakness and fasciculations (twitching of involved muscles); muscles weaken, atrophy; client complains of progressive fatigue; usually involves hands, shoulders, upper arms, and then legs Atrophy of tongue and facial muscles result in dysphagia and dysarthria; emotional lability and loss of control occur 50% of clients die within 2 ² 5 years of diagnosis, often from respiratory failure or aspiration pneumonia

Collaborative Care
Evaluation to make the diagnosis Referrals for home health support; Client needs to make decisions regarding gastrostomy tube, ventilator support

Diagnostic Test
Testing rules out other conditions that may mimic early ALS such as hyperthyroidism, compression of spinal cord, infections, neoplasms EMG to differentiate neuropathy from myopathy Muscle biopsy shows atrophy and loss of muscle fiber Serum creatine kinase if elevated (non-specific) Pulmonary function tests: to determine degree of respiratory involvement

Medications
Rilutek (Riluzole) antiglutamate Prescribed to slow muscle degeneration Requires monitoring of liver function, blood count, chemistries, alkaline phosphatase

Nursing Care
Help client and family deal with current health problems Plan for future needs including inability to communicate

Nursing Diagnoses
Risk for Disuse Syndrome Ineffective Breathing Pattern: may require mechanical ventilation and tracheostomy

Home Care
Education regarding disease, community resources for health care assistance and dealing with disabilities

Client with Creutzfeldt-Jakob disease
Rapid progressive degenerative neurologic disease causing brain degeneration without inflammation Transmissible and progressively fatal Caused by prion protein: transmission of prion is through direct contamination with infected neural tissue Rare in USA affecting persons 55 - 74 Variant form of CJD is ´mad cow diseaseµ: believed transmitted by consumption of beef contaminated with bovine form of disease; none identified in USA as of yet Pathophysiology: spongiform degeneration of gray matter of brain

Manifestations
Onset: memory changes, exaggerated startle reflex, sleep disturbances Rapid deterioration in motor, sensory, language function Confusion progresses to dementia Terminal states: clients are comatose with decorticate and decerebrate posturing

Diagnostic Tests
Clinical pictures, suggestive changes on EEG and CT scan Similar to Alzheimers in early stages Final diagnosis made on postmortem exam

Nursing Care
Use of standard precautions with blood and body fluids Support and assistance to client and family

Client with Guillain-Barre Syndrome
Acute inflammatory demyelinating disorder of peripheral nervous system characterized by acute onset of motor paralysis (usually ascending) Cause is unknown but precipitating events include GI or respiratory infection prior, surgery, or viral immunizations 80 ² 90% of clients have spontaneous recovery with little or no disabilities 4 ² 6% mortality rate, and up to 10% have permanent disabling weakness Characterized by progressive ascending flaccid paralysis of extremities with paresthesia and numbness 20 % require mechanical ventilation due to respiratory involvement

Guillain-Barre Syndrome

Pathophysiology
Destruction of myelin sheath covering peripheral nerves as result of immunologic response Demyelinization causes sudden muscle weakness and loss of reflex response

Manifestations
Most clients have symmetric weakness beginning in lower extremities Ascends body to include upper extremities, torso, and cranial nerves Sensory involvement causes severe pain, paresthesia and numbness Client cannot close eyes Paralysis of intercostals and diaphragmatic muscle can result in respiratory failure Autonomic nervous system involvement: blood pressure fluctuations, cardiac dysrhythmias, paralytic illness, SIADH, urinary retention Weakness usually plateaus or starts to improve in the fourth week with slow return of muscle strength

Collaborative Care
Ensuring adequate respiration and oxygenation Preventing complications due to immobility

Diagnostic Tests
diagnosis made thorough history and clinical examination; there is no specific test CSF analysis: increased protein EMG: decrease nerve conduction Pulmonary function test reflect degree of respiratory involvement

Medications
supportive and prophylactic care Antibiotics Morphine for pain control Anticoagulation to prevent thromboembolic complications Vasopressors as needed

Surgery
may need tracheostomy, if prolonged ventilator support

Plasmapheresis
may be helpful, if used early in the course of disease

Dietary Management
usually requires enteral feeding or total parenteral nutrition

Physical and Occupational Therapy
usually require long-term rehabilitation to regain maximum muscle strength

Nursing Care
involves acute neurological and critical care nursing and rehabilitation

CRANIAL NERVE DISORDER: Trigeminal Neuralgia (Tic Douloureux)  

Neurologic disorder affecting the 5th cranial nerve. Possible fifth cranial nerve root compression Manifested by excruciating, recurrent paroxysms of sharp, stabbing facial pain along the trigeminal nerve.

- Vascular compression and pressure (cause by aging) - Demyelination of trigeminal root - Likely to occur on 5th and/or 6th decade of life - Common to women and with MS

Areas innervated by the three branches of the trigeminal nerve

Signs & Symptoms: - Burning or knife-like pain lasting for 1-15 minutes, usually over the lip or chin and in the teeth. - Pain precipitated by the stimulation of trigger zones during activities such as brushing the hair and eating, or when sitting in a cold draft. - Sudden closure of an eye - Twitching of the mouth

Medications: - Anti-seizure meds Carbamazepine (Tegretol) - To decrease transmission of nerve impulses to the nerve terminals. Nursing Responsibility: - Taken with meals - Serum level should be monitored - Monitor for bone marrow depression (prolonged use of Carbamazepine)

Carbamazepine toxicity - Drowsiness - Nausea & vomiting - Dizziness Aplastic anemia could occur. Other meds: - Gabapentin - Baclofen ² control pain associated with spasm - Dilantin ² oral hygiene needed.

Nursing Diagnosis: - Pain related to nerve root damage. - Self-care deficit - Activity intolerance

Surgical management: - micro-vascular decompression - radio frequency thermal coagulation percutaneous balloon microcompression

Nursing Intervention: - preventing pain - providing post-op care Instruct patient not to rub eyes Artificial tears or eye drops to prevent dryness of the eyes Chew on unaffected area

BELL· PALSY
Unilateral inflammation of the 7th cranial nerve. Results in weakness or paralysis of the facial muscle on the affected side Affects all age ² groups, but occurs most commonly in patients under age 60 Onset is rapid but 80 ² 90% of all patients, it subsides spontaneously, complete recovery in 1 to 8 weeks

Causes: - Hemorrhage - Vascular ischemia - Viral infection/disease (Herpes simplex, Herpes zoster) - Autoimmune disease

Bell·s Palsy
Pathophysiology: An inflammatory reaction occurs around cranial nerve VII, usually at the internal auditory meatus, where the nerves leave bony tissue The inflammatory reaction produces a conduction block that inhibits appropriate neural stimulation to the muscle by the motor fibers of the facial nerve, resulting in the characteristic unilateral or bilateral facial weakness.

Pathophysiologic Chanes/ S & S:
Unilateral facial weakness Drooping mouth & drooling saliva Lost of taste Smooth forehead appearance Impaired ability to close the eye on the weak side Bell·s phenomenon-Upward rolling of the eyes when attempting to close them Excessive tearing Ringing in the ear

Signs & Symptoms: - Facial muscle distorted due to paralysis or weakness - Increase lacrimation or tears - Painful sensation on the face - Speech difficulties - Patient unable to eat on the affected side

Nursing Diagnosis: - Pain r/t inflammed nerve - Impaired verbal communication r/t speech difficulties - Body image disturebance r/t facial paralysis

Medications: - Corticosteroids ² reduces facial nerve edema & improves nerve conduction (Prednisone) - Analgesic ² for pain

Nursing Considerations
Dependent: - hot compress ² causes vasodilation -electrical stimulation ²avoid atrophy facial muscles

of

Nursing Considerations
Independent: - Protection of eye from injury - Protective shield at night - Massage several times a day to regain muscle strength (Upward motion) - Teach patient facial exercises

Nursing Considerations
Give patient frequent and complete mouth care. Remove the residual food that collects between thecheeks and gums Provide support and reassure the patient that recovery is likely within 1 ² 8 weeks Assess the effectiveness of pain medication

Nursing Considerations
Watch for adverse effects of steroids use Apply moist heat to the affected side of the face-to reduce pain Prevent excessive wt loss:
† † †

-have him chew on unaffected side of his mouth -provide a soft, nutritionally balanced diet, eliminating hot foods & fluids -apply a facial sling to improve lip alignment

Offer psychological support

Complications of Bell·s Palsy
Corneal abrasion Infection (masked by steroid use) Poor functional recovery Diagnostic Tests: -based on clinical presentation MRI-rules out tumor Electromyography- 10 days after the onset of S/S

Common Health Problems of the Older Adult

CEREBRO-VASCULAR DISORDER:Stroke/Cerebrovascular Accident (CVA)
Definition: Disruption of the Blood Supply to the Brain-sudden loss of neurologic funtion Note: Middle Cerebral Artery is commonly affected. The second most frequently affected is the internal carotid artery. Classification: ischemic (a thrombus or embolus blocks circulation hemorrhagic (a blood vessel ruptures)

1. 2.

Risk factors: 
         

Increased alcohol intake or cocaine Cardiac disease Cigarrette smoking DM Familial hyperlipidemia Family history of stroke Hx of TIA HPN Obesity,sedentary lifestyle Sickle cell disease Use of hormonal contraceptives

Causes of Stroke: Ischemic 

Thrombosis- occluded bld flow caused by thrombosis of the cerebral arteries supplying the brain or
the intracranial vessels  The most frequent cause of CVA  The most common cause of cerebral thrombosis is atherosclerosis; usually affecting elderly persons.  Tends to occur during sleep or soon after arising.  This may tend to occur among clients with DM, and hypertension. 

Embolism- from thrombus outside the brain, such as in the heart, aorta, or common carotid artery. 
  

The second most common cause of CVA. Most commonly affecting younger people. Most frequently caused by Rheumatic Heart Disease and MI. Symptoms occur at any time and progress rapidly.

Causes of Stroke: Hemorrhagic Stroke 

Hemorrhage- Hemorrhagic Stroke  

Impaired cerebral perfusion from hemorrhage causes infarction, & the bld itself as a space-occupying mass, exerting pressure on the brain tissues Hemorrhage from an intracranial artery or vein, such as HPN, ruptured aneurysm, trauma, hemorrhagic disorder, or septic embolism.

Transient Ischemic Attacks 

Refers to transient cerebral ischemia with  

temporary episodes of neurologic dysfunction. Manifestation include contralateral weakness of the lower portion of the face, fingers, hands, arms, and legs; dysphagia, and sensory impairment. Stoke in evolution refers to development of a neurologic deficit over several hours to days

Pathophysiologic Changes in CVA:-specific manifestations are determined by
the cerebral artery affected, the brain tissue supply by that of that vessel, and the adequacy of the collateral circulation

Aphasia, dysphasia; visual fields deficits; and hemiparesis of affected side (more severe in face & arms)- resulting from thrombosis or hemorrhage of middle cerebral artery Weakness, paralysis, numbness; sensory changes; altered LOC; bruits over carotid artery; and headache caused by thrombosis or hemorrhage of carotid artery Weakness, paralysis, numbness around lips & mouth; visual field deficits, diplopia, nystagmus; poor coordination, dizziness, dysphagia, slurred speech; amnesia, and ataxia resulting from thrombosis or hemorrhage of vertebrobasilar artery.

Confusion, weakness, numbness; urinary incontenece; impaired motor & sensory functions; and personality changes caused by thrombosis or hemorrhage of anterior cerebral artery. Visual field deficits; sensory impairments; dyslexia; cortical blindness and coma resulting from thrombosis or hemorrhage of posterior cerebral artery.

Assessment of CVA: check for: 
 

S&S of increased ICP. Perceptual defects Aphasia Unstable respiration Severe headache Diagnostic procedure results Unilateral neglect

Diagnostic Findings:
CT scan- identifies an ischemic stroke within the first 72 hours of symptom onset or evidence of a hemorrhagic stroke (lesions >1 cm immediately) MRI-assists in identifying areas of ischemia or infarction and cerebral swelling Others: angiography, carotid duplex scan,EEG

Complications:
Hemiplegia ² weakness/paralysis of half the body Cognitive impairement- Aphasia ² maybe expressive or receptive; the partial or tota inability to produce & understand speech Apraxia ² can move but cannot do the purpose; inability to perform complex movements Sensory impairement-Visual changes ² homonymous hemianopsia; Agnosia ² loss of sense of smell
Dysarthria - difficulty in speech articulation due to lack of muscle control Kinesthesia ² loss of sensation (of bodily movement) Incontinence ² maybe fecal/urine; inability to control urination or defecation Shoulder pain Contractures Fluid imbalances Cerebral edema Aspiration Altered LOC Infections such as pneumonia

Nursing Considerations:CVA
Maintain a patent airway and oxygenation: If the pt is unconscious; vomiting- lateral position to prevent aspiration of saliva 

chest pain, shortness of breath, dusky color, tachycardia, fever, and change in sensorium 

If the pt is unresponsive, monitor ABG as ordered

Check v/s & neurologic status: Monitor BP, LOC, pupillary changes, motor and sensory functions, speech, skin, color, temp. Monitor pt for s/s of increased ICP and nuchal rigidity or flaccidity 
 

Monitor F & E balance: Monitor I and O. Administer IVF as ordered Offer bedpan /urinal
.

Watch for s/s of pulmonary emboli: 

Nursing Considerations:CVA 

Ensure adequate nutrition:

Check for gag reflex before offering small oral feedings of semisolod food Teach the client to chew on the unaffected side. If oral feeding is not possible,TPN, NGT feeding, gastrostomy feeding. 
  

Turn the patient frequently, at least q 2 hrs to prevent pneumonia. Perform ROM exercises for affected & unaffected sides. Massage if not contraindicated. Provide meticulous eye care- Instill meds as ordered; patch the affected eye if the pt can·t close eyelid.

Nursing Considerations:CVA 

Compensate for perceptual difficulties.  Care of the client with Hemianopsia.  Approach from the unaffected side.  Place articles on the unaffected side. Promote communication  Care for the client with aphasia.  Say one word at time.  Give simple commands.  Allow the client to verbalize, no matter how long it takes him Give medications as ordered- Tell the pt to watch out for side effects. (ex. Aspirin-GI bleeding 

Assist with rehab
Teach the pt to comb hair, to dress, & to wash Obtain assistive devices ( through the aid of PT/OT) such as walkers, hand bars by the toilet, and ramps as needed Be aware that the pt has a unilateral neglect, in which he fails to recognize that he ha a paralized side- show him how to protect his body from harm Emphasize importance of regular ff-up visits

ANEURYSM

Dilation involving an artery formed at a weak point in the vessel wall

ANEURYSM
Saccular= when one side of the vessel is affected Fusiform= when the entire segment becomes dilated

RISK FACTORS
1. 2. 3. 4.

Atherosclerosis Infection= syphilis Connective tissue disorder Genetic disorder= Marfan·s Syndrome

PATHOPHYSIOLOGY
Damage to the intima and media weakness outpouching Dissecting aneurysm tear in the intima and media with dissection of blood through the layers

ASSESSMENT
1. 2. 3.

Asymptomatic Pulsatile sensation on the abdomen Palpable bruit

LABORATORY:
‡ ‡ ‡ ‡

CT scan Ultrasound X-ray Aortography

Medical Management:
‡ ‡

Anti-hypertensives Synthetic graft

Nursing Management:
‡ ‡

‡ ‡

Administer medications Emphasize the need to avoid increased abdominal pressure No deep abdominal palpation Remind patient the need for serial ultrasound to detect diameter changes

Parkinson·s Disease
Slowly progressive degenerative disorder of basal ganglia function that results in variable combinations of tremor, rigidity, and bradykinesia Onset usually after age 40 men>women

Parkinson·s Disease: deficient in dopamine

Causes:
Exact cause unknown Possible causes: Dopamine deficiency, which prevents affected brain cells from performing their nomal inhibitory function in the CNS Exposure to toxins( manganese dust or carbon monoxide) Repeated trauma to the brain Stroke Brain tumors

Pathophysiology:
Dopamine neurons degenerate, causing loss of available dopamine Dopamine deficiency prevents Affected brain cells from performing their normal inhibitory function Excess excitatory Ach occurs at the synapses Nondopamineric receptors are also involvd Motor neurons are depressed

Pathophysiologic changes/ S&S:
Muscle rigidity, akinesia, and insidious tremor beginning in the fingers (UNILATERAL PILL_ROLL TREMOR) secondary to loss of inhibitory dopamine activity at the synapse- increase during stres or anxiety; decreases with purposeful movement & sleep Muscle rigidity with resistance to passive

Mask-like appearance Gait disturbance-lacks normal parallel motion; may be retropulsive or propulsive Oily skin- secondary to inappropriate regulation of androgen production by hypothalmic-pituitary axis

Pathophysiologic changes/ S&S:
Dysphagia, dysarthria; excessive sweating; decreased GI motility and genitourinary smooth muscle-from impaired autonomic transmission Voice changes Small handwriting Poor judgement, endogenous depression, dementia- from impaired dopamine metabolism, and neurotransmitter dysfunction

Alzheimer·s Disease
Form of dementia characterized by progressive, irreversible deterioration of general intellectual functioning Begins with memory loss, initially subtle until progresses to being more noticeable; course includes deteriorating cognition and judgment with eventual physical decline and total inability to perform ADL

Risk factors
older age female family history Exact cause is unknown; theories include loss of transmitter stimulation, genetic defects, viral and autoimmune cases

Warning signs include
Memory loss affecting ability to function in job Difficulty with familiar tasks Problems with language, abstract thinking Disorientation, changes in mood and personality

Types and Changes in brain
Familial (follows inheritance pattern) and sporadic Early-onset (<65) Older-onset (>65) Loss of nerve cells and presence of neurofibrillary tangles and amyloid plaques Progressive brain atrophy

Manifestations : Stage I
Appears healthy and alert Cognitive deficits are undetected Subtle memory lapses, personality changes Seems restless, forgetful, uncoordinated

Stage II
Memory deficits more apparent Less able to behave spontaneously Wandering behavior, deterioration in orientation to time and place Changes in sleeping patterns, agitation, stress Trouble with simple decisions Sundowning: increased agitation, wandering, disorientation in afternoon and evening hours Echolalia, scanning speech, total aphasia at times, apraxia, astereognosis, inability to write Becomes frustrated and depressed

Stage III
Increasing dependence with inability to communicate, loss of continence Progressive loss of cognitive abilities, falls, delusion, paranoid reactions Average life expectancy is 7 years from diagnosis to death, often from pneumonia, secondary to aspiration

Collaborative Care
No cure Supportive care for client and family

Diagnostic Tests
Diagnosis by ruling out other conditions including depression, hypothyroidism, infection, stroke EEG shows slow pattern in later stages of disease MRI and CT scan: shrinkage of hippocanthus Positron emission tomography (PET):visualizes brain activity and interactions Folstein Mini-Mental Status: instrument reflecting loss of memory and cognitive skills

Medications
Cholinesterase inhibitors used to treat mild to moderate dementia Tacrine hydrochloride (Cognex) Donepezil hydrochloride (Aricept) Rivastigmine (Exelon) Medications to treat depressions Tranquilizers for severe agitation Thioridazine (Mellaril) Haloperidol (Haldol) Antioxidants: vitamin E, anti-inflammatory agents, estrogen replacement therapy in women

Complementary Therapy
Massage, herbs, ginko biloba, Coenzyme Q10 Art therapy, music, dance

Nursing Care &Health Promotion
Intensive, supportive nursing interventions directed at physical and psychosocial responses to illness Maintain functional abilities Maintain safety of client and caregiver

Nursing Diagnoses
Impaired Memory Include written or verbal reminders Use cues to deal with memory loss Chronic Confusion Anxiety Hopelessness Caregiver Role Strain

Home Care
Education regarding disease, anticipation of needs, use of memory cues, support groups and peer counseling Refer to home health agencies, family support, group support

Common Health Problem that occur Across the Life Span

SEIZURE DISORDER
Sudden explosive and disorderly discharge of cerebral neurons abnormal and excessive discharge of neurons in the brain Types of seizures:
† grand

mal † petit mal † febrile seizures † status epilepticus

Petit mal
No aura 10-20 seconds Common to children as well as adult Little tonic-clonic movements Cessation of ongoing physical activities

Jacksonian
With aura With organic lesion Group of muscle affectation

Psychomotor Seizure
With aura With psychiatric involvement Characterized with mental clouding Violence, antisocial acts

Febrile Seizure
Related to temperature Present among children

Status epilepticus
Prolonged seizure state Can occur in any type of sizure Rapid successions with no full consciousness in between Brain damage can occur; most life threatening in tonicclonic seizures Common to clients who are in coma Related to medication

Primary Seizure Disorder (Epilepsy) Idiopathic No apparent structural changes in the brain Secondary Epilepsy Characterized by structural changes or metabolic alterations of the neuronal membranes that caused increased automacity

Causes of Seizures:
Idiopathic- two-thirds of all seisure disorders Anoxia Birth trauma (inadequate supply of O2 supply to the brain, bld incompatibility, hemorrhage) Brain tumors Drug or alcohol abuse or rapid withrawal from abused drugs Febrile illness Genetic predisposition Head injury or trauma Infectious diseases Ingestions of toxins( lead, mercury, or carbon monoxide) Metabolic disorders, such as hypoglycemia or hypoparathyroidism Perinatal infections

Pathophysiology:
Some neurons of the brain may depolarize easily or hyperexcitable. On stimulation, these neurons fires locally or throughout the cerebrum and spreads electric current to surrounding cells. Cells fire in turn and the impulses cascades to one side of the brain ( a partial seizure), both sides of the brain (a generalized seizure), or the cortical, subcortical, and brain stem areas.

Pathophysiologic changes:
Recurring seizures, possibly of more than one type ( hallmark of epilepsy) Visual, olfactory, or auditory hallucinations; sweating or flushing; dream states; anger, or fear reactions resulting from simple partial seizures Altered consciousness , such as amnesia for events around the time of the seizure, resulting from complex partial seizures Movement and muscle involvement resulting from tonic-clonic or myoclonic seizures Brief changes in LOC without motor involvement due to absence sizures

Complications:
Hypoxia or anoxia from airway occlusion Traumatic injury Brain damage Depression and anxiety

Diagnostic Tests:
CT scan or MRI- reveals abnormalities EEG- reveals paroxysmal abnormalities in tonic-clonic seizures, high, fast voltagespikes are present in all leads In absence seizures, rounded spike wave complexes are present Note: a negative EEG doesn·t rule out epilepsy because the abnormalities occur intermittently

Skull x-ray may show evidence of fractures or shifting of the pineal gland, bony erosion, or separated sutures Serum chemistry bld studies may reveal hypoglycemia, electrolyte imbalances, and elvated liver enzyme & alcohol level

Treatment
Drug TherapyEx. Phenytoin (Dilantin) carbamazepine (Tegretol), phenobarbital (Barbita, Luminal) ² for generalized tonic clonic seizures and complex partial seizures Valproic acid (Depakene), clonazepam (Klonopin) for absence seizures

If drug therapy is inefective, surgery to remove a demonsrated focal lesion, or to remove the underlying cause (tumor, abscess) I.V. diazepam ( valium), lorazepam (Ativan) phenytooin, or phenobarbital for status epilepticus Dextrose- for hypoglycemia Thiamine-for chronic alcoholism or withdrawal

Nursing Considerations
Patent airway Oxygenate as needed Raise siderails Ensure safety-during seizure:
† † † † † †

Avoid restraining the pt Help the pt to a lying position Loosen any tight clothing Clear the area of hard objects Don·t place anything into the pt·s mouth to prevent lascerating the mouth & lips or displace teeth If vomiting occurs, turn the head to provide an open airway

After the seizure subsides, reorient the patient to time & place; inform him that he had a seizure Companion at bedside Meds as ordered

Increased Intracranial Pressure
ICP- the pressure exerted within the intact skull by the intracranial volume-about 10% blood,10% CSF, & 80% brain tissue. Causes : head injury CVA tumors HPN Pathophysiology: ^ICPthe brain will compensate by: limiting blood flow to the head displaces CSF into the spinal canal ncreases absorption or decreases production

If ICP remains high, there will be loss of autoregulatory mechanism which will lead to passive dilation, increased cerebral flow, venous congestion. Further increase in ICP will result to cellular hypoxia and eventually, brain death.

Major Types of Herniation

Increased Intracranial Pressure
S&S: Increased HA Nausea &Vomoting Cushing·s triad Restlessness Eye involvement Altered LOC Sensory dysfunction Elimination problem Decorticate/decerebrate

NURSING MANAGEMENT OF INCREASED ICP:
Determine airway patency Elevate HOB Check VS/neuro assessment Record I&O Enema restriction Avoid coughing,vomiting, restraints, stress ulcer,suctioning Seizure precaution Edema reduction Diuretics

Craniocerebral Trauma (Head Injury) 


Involves injury to the scalp, skull, and/or brain tissues. Types of Brain Injury 
  

Concussions. Jarring of the brain and its sudden, forceful contact with the rigid skull. There is transient period of unconsciousness. Contusion (bruising). A structural alteration characterized by extravasion of blood cells. Laceration. Tearing of tissue caused by sharp fragment or object or shearing force. Compression of the Brain. Result from depressed fracture causing edema and hemorrhage.

Assessment 
 

Sign and symptoms of increased ICP. CSF leakage from ears and nose. Battle·s sign (hematoma at the mastoid process) in basilar head trauma.

Management 
 

Care for the client with increased ICP. Monitor drainage from ears and nose. Monitor for signs and symptoms of meningitis, atelectasis, pneumonia, UTI.

Intracranial Tumors  

Intracranial tumors may be classified as: gliomas, meningiomas, neuromas, hemangiomas. Gliomas account for about 50% of all brain tumors.

Assessment 

Frontal lobe
Personality disturbance  Inappropriate affect  Indifference of bodily functions  

Precental gyrus 

Jacksonian seizures Visual disturbances preceeding convulsions. 

Occipital lobe  

Temporal lobe 
Olfactory,

visual or gustatory hallucinations.  Psychomotor seizures with automatic behavior. 

Parietal lobe
to replicate pictures.  Loss of right-left discrimination 
Inability

Management 


Care for the client with increase ICP. Surgery 


Supratentorial craniotomy (post-op) 
   

Semi-fowler·s position Flat position; turn to sides, avoid supine position for the first 48 hours. Avoid neck flexion. Report immediately for presence of yellowish drainage on the head dressing. An increase in urine output may herald onset of diabetes insipidus. Test the urine for glucose and acetone when steroids are administered.

Infratentorial craniotomy

Spinal Cord Injury
complete or partial disruption of nerve tracts and neurons Causes :
-

† infection † trauma † injury

Signs and symptoms
Cervical ²respiratory diff, quadriplegia Thoracic- paraplegia Lumbar ² flaccid paralysis Sacral ² loss of erection, ejaculation

Nursing Asessment:
Injury; treatment given at scene † Neurologic assessment: Document findings † Vital signs; respiratory status † Movement and sensation below injury level † Signs
†

Worsening neurologic damage  Respiratory distress  Spinal shock 

Nursing Diagnoses:
Ineffective breathing pattern † Ineffective airway clearance † Neuropathic pain † Impaired physical mobility † Anxiety † Risks
†

Impaired gas exchange  Disuse syndrome  Ineffective coping 

Medical Management
† † † †

Cervical collar; cast or brace; traction; turning frame IV; stabilization of vital signs Corticosteroids Surgical intervention Surgery to 
 

Surgical Management
†

Remove bone fragments Repair dislocated vertebrae Stabilize the spine

Management
Maintain airway patency Immobilize Suction PRN Position Nutrition Elimination hygiene Drugs

Evaluation:
† Adequate † Pain

breathing

relief † Mobility using minimal assistive devices † Reduced complications from inactivity † Coping with the challenge of rehabilitation

Infectious Neurologic Disorders
Meningitis Brain Abscess Herpes Simplex Virus Encephalitis Arthropod-Borne Virus Encephalitis Fungal Encephalitis Creutzfeldt-Jakob and New-Variant CreutzfeldtJakob Disease

Infectious Process
Bacterial meningitis and Infectious Enceohalitis Pyrogenic or purulent infection that involves the pia matter and arachnoid matter layers of the meninges.

Infection of Meninges

Pathogens
Under 2 months :E-coli, Group B streptococcus, Listeria, Haemophilus influenza type B, and Streptococcus pneumonia Beyond neonate: Strep, Haemophilus, Neisseria.

Contributing History
Otitis Sinusitis Mastoiditis Post skull fracture Meningiocele PROM Premature infant Sepsis / bacteremia

Clinical Manifestations
Poor feeding Hypothermia / hyperthermia Irritability Apnea Bulging fontanel Look sick

Clinical Manifestations
Older Child
† High

fever † Headache † Nuchal rigidity / stiff neck † + Kernigs = inability to extend legs † + Brudzinski sign = flexion of hips when neck is flexed † Purple rash (check for blanching)

Assessment for Positive Meningitis

Kernig Sign
Raise child¶s leg with knees flexed. Extend leg at the knee. Resistance or pain = + sign. Ball & Bindler

Brudzinski Sign
Flex the head while Child in a supine position. + Brudzinski = involuntary flexion of Ball & Bindler knees.

Septic Looking

Ball & Bindler

Purple Rash

Bowden & Greenberg

Characteristic purpuric lesions of meningococcal meningitis.

Diagnostic Tests
+ Spinal fluid + Blood Culture

Management
IV antibiotics Dexamethasone to decrease meningeal inflammation and hearing loss Monitor Gentamicin blood levels

Interventions
Droplet precautions Isolation X 24 hours Vital signs Neuro checks / palpate fontanel Monitor fluids to prevent fluid overload Head circumference Pain management / quiet environment

Droplet Protection
If patient is a rule out meningitis the nurse should wear a mask when helping with diagnostic tests.

Outcomes
Unfavorable outcomes
† Young

age † Delay in treatment † Coma † Focal neurologic signs † Poor clinical course

Follow-up
BAER hearing test in hospital and 3 to 6 months later Developmental testing Watch for learning disabilities

Brain Injuries
Closed (blunt) Brain Injury Open Brain Injury Concussion Contusion Diffuse Axonal Injury
Intracranial Hemorrhage
† Epidural

Hematoma † Subdural Hematoma

Intracerebral Hemorrhage and Hematoma

Pathophysiology

Subdural Hematoma
Shear force injury created by impact can cause tearing of bridging vessels. Falls, assaults, MVA, Shaken Baby Syndrome. Children under 1 year

Clinical Manifestations
or changes in LOC Vomiting Headache Retinal hemorrhages Pupil on side injury fixed and dilated Seizures

Retinal Hemorrhages

Normal retinal

Retinal hemorrhage

Subdural Hematoma
CT scan to confirm diagnosis Subdural tap

Epidural Hematoma

Depressed Skull Fracture
Six-year old hit by auto while riding his bike.

Depressed Skull Fracture
Part of the skull is actually sunken in from trauma. May occur with or without a cut in the scalp. Surgical intervention is needed to correct the deformity.

Basilar Skull Fracture
Most serious type of skull fracture. Involves a break in the bone at the base of the skull. Child has bruises around their eyes and a bruise behind the ear. May have clear fluid draining from their nose or ears. Need close observation in hospital.

Battle·s Sign

Battle¶s Sign

Nursing Intervention
Secure the injured site. Prevent further injury by imobilizing, covering, applying pressure on bleeding sites. Assess the extent of the injury including spinal and neurologic involvement. If spinal involvement is negative, place patient on a high fowler·s position Loosen clients clothing and allow optimal ventilation Place client on NPO until vomiting is unlikely to ocure.

Neurologic Diseases that result from viral infections or neurotoxins

Postpoliomyelitis Syndrome
Complication of previous poliomyelitis virus (epidemic occurred in USA during 1940·s and 1950·s); persons who recovered are reexperiencing manifestation of acute illness in their advanced age Pathophysiology: Process is unknown Manifestations: Fatigue, muscle and joint weakness, loss of muscle mass, respiratory difficulties, and pain Diagnosis: By history and physical examination Treatment: Involves physical therapy and pulmonary rehabilitation Nursing Care: Involves emotional support and interventions to deal with dysfunction; ADL, safety are including in interventions

Rabies
Rhabovirus infection of CNS transmitted by infected saliva that enters the body through bite or open wound Critical illness almost always fatal Source often is bite of infected domestic or wild animal Incubation is 10 days to years

Rabies
Manifestations occur in stages Prodromal: wound is painful, various paresthesias, general signs of infection; increased sensitivity to light, sound, and skin temperature changes Excitement stage: periods of excitement and quiet; develops laryngospasm and is afraid to drink (hydrophobia), convulsions, muscle spasms and death usually due to respiratory failure

Rabies
Collaborative Care Animal that bit person is held under observation for 7 ² 10 days to detect rabies Sick animal are killed and their brains are tests for presence of rabies virus Blood of client may be tested for rabies antibodies

Rabies
Post-exposure treatment Rabies immune globulin (RIG) is administered for passive immunization Client often has local and mild systemic reaction; treatment is over 30 days Treatment of client with rabies: involves intensive care treatment Health Promotion Vaccination of pets Avoid wild animals, especially those appearing ill Follow up care for any bites

Tetanus (lockjaw)
Disorder of nervous system caused by neurotoxin from Clostridium tetani, anaerobic bacillus present in the soil Contract disease from open wound contaminated with dirt, debris Has high mortality rate Incubation is usually 8 ² 12 days Manifestations Stiffness of jaw and neck and dysphagia Spasms of jaw and facial muscles Develops generalized seizures and painful body muscle spasms Death occurs from respiratory and cardiac complications

Tetanus (lockjaw)
Diagnosis is made on clinical manifestations Clients with disease are treated in intensive care with antibiotics, chlorpromazine (Thorazine) and diazepam (Valium ) for muscles spasms Health Promotion Active immunization with boosters given at time of exposure Passive immunization is given to persons who are not adequately immunized

Botulism
Food poisoning caused by ingestion of food contaminated with toxin from Clostridium botulinum, anaerobic bacteria found in soil Contracted by eating contaminated foods usually improperly canned or cooked Untreated death rate is high Pathophysiology: Bacteria produce a toxin, which blocks release of acetylcholine from nerve endings causing respiratory failure by paralysis of muscles

Botulism
Manifestations Visual disturbances Gastrointestinal symptoms Paralysis of all muscle groups Effecting respiration Diagnosis Based on clinical picture Verified by laboratory analysis of client·s serum and stool Testing the suspected food

Botulism
Treatment Administration of antitoxin Supportive treatment including mechanical ventilation and systemic support in intensive care unit Health Promotion Teaching clients to process foods properly when home canning Boiling foods for 10 minutes which destroys the toxin Not eating spoiled foods

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