neurological disorders

CARE OF CLIENTS WITH

NEUROLOGICAL DISORDERS

Prepared by: Jessica M. Saldana RN., MAN

The Spinal Cord

Peripheral Nervous System

ANATOMY AND PHYSIOLOGY OF THE NERVOUS SYSTEM:

The neuron is the structural and functional unit of the nervous system.

Anatomy and Physiology

The nervous system has three major divisions, the central nervous system (CNS), the peripheral nervous system (PNS) and the autonomic nervous system (ANS).

The CNS is composed of the brain and the spinal cord. It regulates the higher level processes.

The PNS is composed of 12 pairs of cranial nerves and 31 pairs of spinal nerves. It provides pathways to the CNS.

The ANS (sympathetic and parasympathetic nervous system coordinates involuntary activities, eg., digestion, breathing


The Central Nervous System (CNS)

1. The Brain

a. Cerebrum. Is divided into 2 sections called cerebral hemispheres.

The outermost layer of the cerebrum is called the cerebral cortex.


The falx cerebri divides the brain into right and left cerebral hemispheres; the commissural tracts known as corpus collosum connects the 2 cerebral hemispheres.

Both the left cortex and the right cortex interpret sensory data, stores memories, learn and form concepts.

The left cortex has dominance for systematic analysis language and speech, mathematics, abstraction and reasoning.

The right cortex has dominance for assimilation of sensory experiences, such as visual- spatial information and activities such as dancing gymnastics, music and art appreciation.


The cerebral cortex is composed of gray mater formed into raised convolutions called gyri; the shalow grooves between the gyri are called sulci.


The sulci divide the cerebral cortex into five lobes: Frontal lobe Parietal lobe Temporal lobe Occipital lobe Central lobe (insula)


The frontal lobe has the following functions: Controls voluntary motor

activity precentral gyrus or motor cortex)

Expressive (motor) speech- ability to speak clearly (Broca’s area). Damage to this area leaves the client unable to speak clearly. (expressive aphasia).


The prefrontal areas control

1) Concentration(attention over time)

2) Motivation3) Ability to formulate or

select goals4) Ability to plan (e.g. future

planning)5) Ability to initiate, maintain,

or terminate actions.


6) Ability to self- monitor7) Ability to use feedback (“executive feedbacks”)8) Reasoning, problem-solving activities, emotional stability.9) Development of personality10) Sense of humor The parietal lobe has the following functions:

1) Sensory perception (tactile sensations like temperature, touch, pain, pressure)- post central gyrus.2) Concept formation and abstraction.3) Spatial Orientation and awareness of size and shapes (stereognosis)and body position (proprioception)-right pareital lobe.


4) Right –left orientation and mathematics-left parietal lobe.

The temporal lobe has the following functions:

1) Auditory receptive area-ability to hear.

2) Auditory association areas- ability to store spoken language memories (left Temporal); sound memories that are not language like music, various animal sounds, other noises (right temporal). Damage to these areas leaves client unable to understand spoken or written language or to recognize music or others environmental sounds.


3) Wernicke’s area facilitates understanding language. Damage to this area results to receptive or auditory aphasia.

The occipital lobe has the following functions:

1) Visual receptive (interpretation) area.

2) Visual association areas- storage of visually recognize and understand the environment.

3) Visual speech center enables a person to read. Damage to this area leaves the client unable to read (Alexia).


The central (insula) lobe. Nerve fibers for taste pass through the parietal lobe to the insular lobe. Many association fibers leading to other parts of the cerebral cortex pass through this lobe.

b. Hippocampus. Is a part of the medial section of the temporal lobe. It plays a vital role in the process of the memory. Three levels of memory have been identified: Short-term (recent) memory is lost after seconds or

minutes. Intermediate memory lasts days and weeks and

eventually lost. The outermost layer of the cerebrum is called the cerebral cortex.


The hippocampus assists in the conversion of short term memory into the intermediate and long-term memory in the thalamus.

c. Basal ganglia. Is composed of layers of gray mater buried deep in the cerebral hemispheres. These structures include nucleus Putamen, globus pallidus, substantia nigra, subthalmic nucleus.The basal ganglia is important in controlling

complex motor activity.


d. Diencephalon. Is composed of the thalamus and the hypothalamus. The thalamus channels all sensory information

except smell to the appropriate cortical cells. The hypothalamus regulates the autonomic nervous

system (ANS) functions such as heart rate, blood , pressure, water and electrolyte balance, stomach and intestinal motility, glandular activity, body temperature, hunger, body weight and sleep- wakefulness. It also serves to be the master over the pituitary gland by releasing factors that stimulate or inhibit pituitary gland output.


e. Limbic system. Is composed of the medial portion of the frontal lobe, temporal lobe (hippocampus), thalamus, hypothalamus and the basal ganglia. It is the center for feelings and control of emotional

expression (fear, anger ,pleasure, sorrow). The temporal lobe component of the limbic system

plays essential role in the interpretation of smell.


f. Brain Stem. Is composed of the midbrain, pons and medulla oblangata.The midbrain integrates visual and auditory reflexes.

E.g. if a person sees a wasp towards him, he ducks or twist away (visual reflex). Another example is turning the hear ( ear ) to sound (auditory reflex). The midbrian is also responsible for the righting reflexes, those that keep the head upright and maintain balance or equilibrium.

The pons contains 2 respiratory centers that promote normal rhythm of breathing. The apneustic center prolongs inhalation; the pneumotoxic center contributes to exhalation.


The medulla oblangata contains cardiac centers that regulate heart rate; vasomotor centers that regulate blood pressure; respiratory centers that regulate breathing. It also contains reflex centers for coughing, sneezing, swallowing, and vomiting.

g. Reticular formation. Assists in the regulation of skeletal motor movement and spinal reflexes. It also filters incoming sensory information to the cerebral cortex.One component of the reticular formation, the reticular

activating system controls the sleep-wake cycle and consciousness.


h. Cerebellum. IS composed of gray mater and white matter. It controls balance (equilibrium) and posture.It controls voluntary (purposeful) motor activities

and position of body parts.Most of the tracts in the cerebellum do not cross.

Therefore, the right cerebellum hemisphere predominantly affects the right (ipsilateral) side of the body and vice versa.


• Left and Right Brain Functions Dominant Hemisphere (Left)

Language and logical operations

1)Number skills

2)Written language

3)Reasoning

4)Spoken language

5)Scientific skills

6)Right-hand control


Right Hemisphere Emotions, artistic and spatial skills

1) Insighte.g. How does a client recognize implication of illness?How would the client respond to a given situation ( e.,) house on fire)?

1) Forms (3 dimensions)2) Art awareness3) Imagination4) Music awareness5) Left-hand control


2. The Spinal Cord

a. The spinal cord is composed of ascending and descending pathways.

b. The ascending pathways (affarent fibers) are sensory fibers. They carry impulses TO THE BRAIN.

c. The descending pathways (efferent fibers) are motor fibers. They carry impulses to the brain.

d. The spinal cord is the center for reflex acts.

e. It is the origin of ANS.


f. The craniosacral segment is the origin of the parasympathetic nervous system. The thoracolumbar segment is the origin of the sympathetic nervous system.

g. Damage to the spinal cord causes paralysis and loss of reflexes below the area of lesion. E.g. Cervical spinal cord injury results to qaudriplegia ( paralysis of the four extremities)

h. Protective and Nutritional structures Cranium and the vertebrae column

The cranium is composed of eight bones that fuse in early childhood. The fused junctions are called sutures.


The vertebral column consist of 7 cervical vertebrae, 12 thorasic vertebrae, 5 lumbar vertebrae, 5 sacral vertebrae fused into a sacrum and 4 coccygeal vertebrae fused into a coccyx.

Meninges. Consists on 3 membranes that envelope the brain and spinal cord. These are the pia mater, arachnoid and dura mater. The pia mater is a the tissuvascular layer of

connective tissues. It supports blood vessels passing through the tissues of the brain and spinal cord.

The arachnoid is a thin layer of connective tissue,


The arachnoid is a thin layer of connective tissue. The space between the arachnoid and the pia mater is called subarachnoid space. Cerebrospinal fluid (CSF) flows through this space.

The cranial dura mater is a tough, non-stretchable vascular membranes. The subdural space is the potential space between the inner dura matter and the arachnoid. The epidural space is between the dura matter and the periosteum


Reflex mechanisms. Reflex responses are conscious automatic response to internal and external stimuli. The reflex centers are the spinal cord (flexion and extension) and the brain stem ( heart rate, breathing, blood pressure, swallowing, sneezing, coughing and vomiting).

Cerebrospinal fluid and ventricular system. CSF is a clear, colorless fluid. Approximately 100 to 160

ml. in amount. The CSF is primarily produced by the choroid plexus of the

lateral ventricles (2/3 of the CSF). Approximately, 500 ml. of CSF is produced per day. But

normally, it is absorbed in the blood at the same rate at which it is formed.

Anatomy and Physiology The ventricular system is a series of activities within the brain. CSF Flow

Lateral ventricles

Foramen of Monro

Third ventricles

Aquduct of Sylvius

Foiurth ventricle

Foramina of LuschkaForamen of Megendie

Subarachnoid space(Cisterna Magna) behind medulla, below the cerebellum Brain spinal cord

CSF circulates upward into the superior sagittal sinus where it is absorbed across the arachnoid villi


Blood Supply of the Braina. The brain receives 750 to 900 ml. of blood flow per

minute.b. The vertebral arteries and the internal carotid arteries

provide the arterial supply to the brain.c. The vertebral arteries join to form the basillar artery.

The basilar artery bifurcates to form 2 posterior cerebral arteries.

d. The vertebral artery system supplies the brain stem, the cerebellum, the lower portion of the diencephalon and the medial and inferior regions of the temporal and occipital lobes (posterior lobes)


e. The internal carotid arteries bifurcate into the anterior and middle cerebral arteries.

f. The circle of Willis is a ring of blood vessels at the base of the brain. It is formed by the posterior cerebral arteries posterior communicating arteries, internal carotid arteries, and anterior communicating branches.

g. The internal carotid arteries supply the upper diencephalon, basal ganglia, lateral temporal, occipital lobes and parietal and frontal lobes ( anterior brain).


h. The middle cerebral arteries supply large portions of the frontal, parietal, temporal, occipital and insular lobes and basal ganglia and thalamus.

i. The anterior cerebral arteries supply the medial portions of the frontal and parietal lobes and the upper basal ganglia.

j. Most of the venous blood from the head returns to the heart through internal jugular veins, the external jugular veins, and the vertebral veins.


The Peripheral Nervous system (PNS) It consists of pathways of nerve fibers.

a.Sensory (affarent) neurons. Conduct impulses to the brain and the spinal cord.

1.Spinal Nerves. There are 31 pairs of spinal nerves; 8 pairs of

cervical nerves; 12 pairs of thoracic nerves, 5 pairs of lumbar nerves, 1 pair of coccygeal nerves. (8-12-5-5-1)


The 3 major plexus formed from the peripheral nerves are as follows:

1) Cervical plexus: supplies the muscles and skin of the neck and branches to form the phrenic nerve, which innervates the diaphragm.

2) Brachial plexus: supplies the muscles and skin of the shoulder, axilla, arm, forearm and hand. It branches to form the ulnar, median and radial nerves.

3) Lumbosacral plexus: supplies sensory and motor impulses to the muscles and skin of the perineum gluteal region, thighs, legs and feet. Its branches include pudendal, gluteal, femoral, sciatic, tibial and common fibular nerves.


The Autonomous Nervous System (ANS)The autonomic nervous system is the part of the PNS

that coordinates involuntary activities, such as the visceral functions, smooth and cardiac muscle changes, and glandular responses.

The ANS has 2 divisions: the sympathetic and parasympathetic nervous systems.

The sympathetic nervous release norephineprine.The parasympathetic nerves release acetylcholine

CRANIAL NERVESCranial Nerves Functions Abdominal Findings

Olfactory Smell Anasomia(absence of smell

Optic Vision Papilledema; blurred vision; scotoma; blindess

Oculomotor Pupil constriction elevation of the upper lid

Anisucuria;pinpoint pupils; fixed dilated pupils

Trochlear Eye movement; controls superior oblique muscles

Nystagmus

Trigemenal Controls muscles of mastication; sensations for the entire face and cornea

Trigeminal Neuralgia (Tic douloureux)

Abducens Eye movement; control the lateral rectus muscles

Diplopia;ptosis of eyelid

Cranial NervesCranial Nerve Functions Abnormal Findings

Facial Controls muscles for facial expression; anterior 2/3 of the tongue

Bell’s palsy ageusia (loss of sense of taste) on the anterior 2/3 of the tongue.

Acoustic Cochlear branch permits hearing; vestibular branch helps maintain equilibrium

Tinnitus: Vertigo

Glossopharyngeal Controls muscles of the throat; taste of posterior 1/3 of the tongue

Loss of gag reflex, drooling of saliva dysphagia, dysphonia, posterior third ageusia

Vagus Nerve Controls muscles of the throat, Parasympathetic Nervous System stimulation of thoracic and abdominal organs.

Loss of gag reflex, drooling of saliva dysphagia, dysarthria, bradycardia, increase HCL secretion

Cranial NervesCranial Nerves Functions Abnormal Findings

Spinal Accessory Controls sternocleidomastoid and trapezius

Inability to rotate the head and move the shoulders.

Hypoglossal Movement of the tongue Protrusion of the tongue or deviation of the tongue to one side of the mouth

EFFECTS OF THE SYMPATHETIC AND PARASYMPATHETIC NERVOUS SYSTEM ON

ORGANS

Organ Effects of Sympathetic Stimulation

Effects of Parasympathetic

Stimulation

Eye Pupil Ciliary muscle

Dilation (alpha)*Slight relaxation ( far vision)

ConstrictionConstriction (nrear vision)

Glands Nasal Lacrimal Parotid Submandibular Gastric Pancreatic

Vasocontriction and slight secretion

Stimulation of copius secretions(containing many enzymes for enzyme secreting glands


ORGANS



Stimulation

Sweat Glands Copius sweating Sweating on palms of hands

Heart Muscle

Coronaries

Increased rate (beta1)Increased force of contraction (beta1)

Dilated (beta2);Constricted (alpha)

Slowed heart rateDecreased force of contraction (especially of atriaDilatation

Lungs Dilated (beta2) Constriction


ORGANS



Stimulation

Gut Lumen

Sphincter

Decreased peristalsis and tone (beta2)Increased tone (alpha)

Increased peristalsis and toneRelaxation (most of the time)

Liver Gluconeogenesis, glycogenolysis (beta2)

Slight glycogen synthesis

Gallbladder and bile ducts

Relaxation Contraction

Kidney Decreased output and renin secretion

None



Stimulation

Bladder Detrusor

Trigone

Relaxation ( slight)(beta2)Contraction (alpha)

Contraction

Relaxation

Penis Ejaculation Erection

Systemic arterioles Abdominal viscera Muscle

Constriction (alpha)Constriction

None


ORGANS

Normal functioning of the nervous system requires the following:

1. Oxygen Supply. The brain requires 20 % of the oxygen in the body.

2. Glucose supply. The brain requires 65 to 70 % of the glucose in the body. The cardiac output.

3. Blood supply. The brain requires 1/3 of the cardiac output.

4. Acid-base balance. Acidosis causes cerebral vasodilatation and increases

intracranial pressure (ICP). It also a CNS depressant and may lead to coma.

Alkalosis causes cerebral vasoconstriction and Increases intracranial pressure. It also a CNS depressant and may lead to coma

Normal functioning of the nervous system requires the following:

5. Blood-brain barrier. Intact blood-brain barrier protects the brain from certain drugs, chemicals and microorganisms.

6. Cerebro spinal fluid( CSF) Volume . CSF cushions the brain and determines the ICP.CSF cushions and nourishes

NEUROLOGIC ASSESSMENT

1. Mental Status Assess orientation and memory (consider educational

background) Orientation involves people, time and place. Memory includes short-term (immediate recall), recent and

remote memory.

2. Level of consciousness (LOC). It is the single most sensitive indicator of changes in the neurlologic status of a client.

The levels of consciousness are as follows:a. Level 1 Conscious, coherent, cognitive (3 C’s)b. Level II. Confused, drowsy, lethargic, somnolent, obtunded.

NEUROLOGIC ASSESSMENT

c. Level III Stuporous; responds only to noxious, strong or intense stimuli, e.g. sternal pressure, trapezius pinch, pressure at the base of the nail or supraorbital area; very strong light or very loud sound.

d. Level IV. Light coma: response is only grimace or

withdrawing limb from pain, primitive and disorganized response to painful stimuli.

Deep Coma: absence of response to even the most painful stimuli.

Normal 14-15Lethargy 11-13Stupor: 8-10Coma: 7Deep

Coma: 3

Neurological Assessment

3. Sensory Function Test for sensory function assess the functioning of

the parietal lobe. The tests are done with the client’s eyes closed, e.g.,

placing cold and warm fluid in test tubes over the skin; pricking skin with blunt objects; giving cinnamon to taste ; coffee to smell.

Agnosia is inability to perceive sensory stimuli.


4. Motor Function If the frontal lobe is affected, the client experiences

inability to perform motor activities. Apaxia is inability to perform fine motor

activities( done by fingers) Agraphia is inability to write. Romberg test is done to assess cerebellar function

(sense of equilibrium). The test is done by asking the client to stand with the feet together and eyes closed or the client is asked to walk in a imaginary line.


Normal result of Romberg test is that, the client should be able to stand erect. Slight swaying is normal. If the client falls, this is a positive Romberg that indicates cerebellar function impairment.

Ataxia is uncoordinated movement, characterized by wide base stance and swaying manner of walking.

Assessing motor function includes the following:

a. General appearance. Assess for Presence of involuntary, unpurposeful, and

uncoordinated movements, asymmetry of the face muscle dystrophy.


b. Muscle Power. Assess for Weakness (“paresis) Paralysis (“plegia”)

c. Muscle Tone. Assess for Flaccidity (hypotonicity) Rigidity (hypertenocity)

c. Muscle volume. Assess for Atrophy (loss of muscle volume) Hyperthrophy ( increase in muscle volume


e. Movement. Assess for Bradykenesia ( slow muscle movement not associated

with weakness). Akinesia (absence of muscle movement not associated

with weakness).f. Coordination. Assess by

FTNT (finger-to nose-test) H-K-T ( heel-to-knee-to-toe-test)

f. Station and gait. Station is posture; gait is manner of walking Parkinson’s disease is characterized by shuffling,

festinating gait (tiptoe walking, starting at slow motion, the pace keeps on increasing until client assumes running pace.


5. Reflex Testing. Superficial Reflexes

Pupillary Reflexes Direct light reflex is elicited by applying light

stimulus movement side to side into the pupil; this results to constriction of the pupils.

Consensual light reflex results to stimulus constriction of both pupils even if light is applied to one pupil only.

Accommodation reflex results to constriction of pupils when gaze is shifted from a distant object to a near object.


The pupillary reflexes are represented by PERRLA ( pupils, equal, round, reactive to light, accommodation.)

A fixed and dilated pupil in a client who has had previously reactive pupils is a neurologic emergency. Notify the physician immediately.

Corneal reflex is elicited by touching the cornea with a wisp of cotton, as the client looks toward opposite direction; blinking of the eyes occurs.

Abdominal reflex results to contraction of the side of the abdomen stroked with blunt object.


Cremasteric reflex is elicited by downward stroking of the inner thigh of the male; elevation of the scrotum on the same side occurs; this done only among unconscious males.

Babinski reflex is elicited by stroking the sole of the foot from the heel upwards; plantar flexion (negative Babinski) is the normal result among adults.

Interpretation of Superficial Reflexes 0 absent + slightly present + normally active

Neurological Assessment Deep Tendon Reflexes (DTR’s)

Ankle jerk is produced by tapping the tendon of Achilles; plantar flexion of the foot occurs (also called Tendon of Achilles reflex)

Knee jerk (patellar reflex) is produced by tapping the quadriceps femoris, just below the patella; it results to leg extension

Reflexes to assess meningeal irritation Kernig’s sign. The client in supine position. Flex the

knee, attempt to extend the leg. Pain is experienced. Brudzinski’s reflex. The client is placed in supine

position. Passively flex the neck, spontaneous flexion of the hips occurs. This is more accurate indicator of meningeal irritation than kernig’s sign.

Neurological Assessment Oculocephalic Reflex or Doll’s eye phenomenon.

This is demonstrated by holding the person’s eyelids open and rotating the head from side to side. Positive or normal doll’s eye is demonstrated by conjugate movement of the eyes towards the opposite side.


Oculovestibular Reflex or Caloric Ice Water Test. This is done by irrigating the semi-circular canals of the ear with ice water. It causes conjugate eye movements or nystagmus. This is an accurate method of assessing brainstem functioning.


6. Language and Speech.

The speech centers are as follows: Broca’s area in the left frontal lobe. This is the motor speech

center. This enables a person to speak and make gestures. Impairment of the Borca’s area results to expressive or motor aphasia which is inability to speak and make gestures.

Wernicke’s area in the temporal lobes. This is the auditory speech center. This e sounds nables a person to interpret sounds or language. Impairment of the Wernicke’s area results to receptive or auditory aphasia, which is inability to understand sounds or language.


Global aphasia is inability to use and understand language. This occurs from impairment to both the Broca’s and Wernicke’s areas.

Visual speech center in the occipital lobe. This enables a person to read or interpret symbols. Impairment of the visual speech center results to alexia, which is inability to read.

7. Bowel and Bladder Function The sympathetic nervous system (SNS) which

originates from the thoracolumbar segment of the spinal cord is the inhibitory impulse. Impairment of the SNS leads to bowel and bladder retention.


The parasympathetic nervous system, (PNS) which originates from the craniosacral segment of the spinal cord is the motor impulses. Impairment of the PNS leads to bowel and bladder incontinence.

DISORDERS AFFECTING NERVOUS

SYSTEM

The three common problems among clients with neurologic disorders are as follows:

1. Increased intracranial pressure

2. Seizures

3. Altered level of consciousness

Care of the client with Increased Intracranial Pressure (ICP)• Increased ICP occurs whenever there is increase in the bulk

of the brain.• The bulk of the brain consists of the brain tissues, blood

supply and CSF.• The disorders that increase the bulk of the brain tissues are

called space-occupying lesions. E.g. cerebral tumor, abscess, edema (due to infection or trauma).

• The factors that may increase the blood supply to the brain are cerebral hemorrhage, trombosis, embolism, aneursym, anteriovenous malformation (A-V mal)

• The factors that increase bulk of of CSF are obstruction to the flow of CSF caused by brain tumor or ventricular system defects (hydrocephalus); or over production of CSF caused by tumor in the choroid plexus.

• Increased ICP causes cerebral hypoxia.

Care of the client with Increased Intracranial Pressure (ICP)

• The clinical manifestations of increased ICP are as follows:

Restlessness. Is the initial sign of increased ICP. Headache is due to traction on pain-sensitive brain

structures and on cranial nerves. Nausea and vomiting. Is due to pressure at the

medulla oblangata. Vomiting may be projectile. Diplopia (double vision). Is due to pressure on the

cranial nerve VI (abducens), which controls the lateral rectus muscles of the eyes. Cranial nerve VI is the longest intracranial nerve. Therefore, it is very vulnerable to compression.

Care of the client with Increased Intracranial Pressure (ICP) Altered level of consciousness. Is due to affection of ascending reticular

activating system (ARAS) Vital signs changes. Are due to stimulation of the Cushing’s reflex in

response to cerebral hypoxia: The Cushing’s triad are as follows:a. Blood Pressure

Systolic pressure is elevated. This is due to increased force of cardiac contractility, the body’s attempt to increase cerebral tissue perfusion and oxygenation.

Diastolic pressure remains normal or decreased. This is due to longer time required for the heart to relax.

Widening of pulse pressure. It is more than 40 mm. hg. (pulse pressure is the difference between systolic pressure and the diastolic pressure: S – D = pulse pressure).

a. Pulse rate. Bradycardia ( slow bounding pulse) occurs.b. Respiratory rate, is slow due to involvement of the medulla

oblangata and pons.


The other vital signs changes are as follows:

a. Body temperature. Hyperthermia or hypothermia may occur due to the involvement of the hypothalamus

Pupillary Changes

a. Anisucuria (unequal pupil). Is due to Cranial nerve III (oculomotor) compression. There is ipsilateral (same side) pupil dilatation; e.g. left brain affection, left pupil is dilated.

b. Pinpoint pupils indicates pons involvement.

c. Fixed dilated pupils. Indicates uncal herniation. This causes compression of the brainstem that may result to cardiopulmonary arrest.


Papilledema (Chocked disc). Is due to the compression of the optic nerve.

Laterilizing Sign. This is contralateral (opposite side) loss of motor function due to decussation ( crossing) of motor fibers at the level of medulla oblangata, eg., left brain affection leads to right hemiplegia (paralysis of he right lateral half of the body); right brain affection leads to left hemiplgeia (paralysis of the left lateral half of the body).

Brainstem Function impairmenta. Negative Doll’s eye sign. Dysconjugate movement

of the eyes as the head is moved to pone side.


b. Decortication( flexion , adduction and internal rotation of upper extremities. Lower extremities are extended). This indicates involvement above the mid brain.


c. Decerebration ( extension adduction, and internal rotation of the arms and extension of the lower extremities). This indicates involvement of the brain stem. The signals poor prognosis. The client may have cardiopulmonary arrest, anytime.


d. Oculovestibular Test (Caloric Ice water test). Dysconjugate movement of the eyes occurs in response to irrigation of the ear with cold water.

ICP

Alterations in:

a. Sensory Function (anosia)

b. Motor Function (seizures)

c. Lnaguage and Speech (expressive aphasia, receptive aphasia. A;exia).

d. Bowel and bladder function (retention or incontinence).

Collaborative Management for ICP includes the following:

NURSE ALERT: Increased ICP is an emergency. The cerebral cortex can tolerate hypoxia only for 4 to 6 minutes. The medulla oblangata can tolerate hypoxia only for 10 to 15 minutes.

Collaborative Management for Icreased ICP include the following:

Position: Semi- Fowler’s. Lateral position. The HOB elevation is 15 to 30 degree, maximum of 45 degree. To promote drainage of CSF from subarachnoid space of the spinal cord. This position also promotes maximum lung expansion. CAUTION: do not elevate HOB at 90 degrees. This may cause brain herniation.

Adequate oxygenation. Mechanical ventilation helps promote acid-base. Acidosis and Alkalosis may increase ICP.

Safety. Prevent falls that may result from altered level of consciousness and seizures.

Rest. Physical and emotional stress may further increase ICP.


Avoid factors that increase ICP as follows: Nausea and vomiting Valsalva maneuver, e.g. straining at stool Over suctioning Restraints application Rectal examination Enema Bending or stooping

If coughing and sneezing could not be avoided, follow[through with an open mouth.

Control hypertension. Hypertension reduces cerebral tissue perfusion.


Restrict fluid intake. Limit fluid intake to 1,200 to 1, 500 mls./day to reduce CSF production.

Pharmacotherapy Mannitol, an osmotic diuretic. It reduces cerebral edema

by increasing urine output. Check hourly urine output. Check BP for potential hypotension.

Lasix (Furosemide), a diuretic. It helps reduce cerebral edema by increasing urine output.

Decadron (Dexamethasone), a corticosteroid. It has anti inflammatory effect and reduces cerebral edema. This is the only corticosteroid that can pass through the blood- brain barrier.


Anticonvulsants to prevent seizures. Valium (Diazepam) Dilantin (Phenytoin Sodium) Phenobarbital ( Sodium Luminal) Tegretol (Carbamezapine)

Antacids to prevent G.I. irritation that may be induced by Decadron (dexamethasone).

Histamine- H2 receptor antagonists. To prevent stress ulcer (Cushing’s ulcer), e.g. Zantac (Ranitidine).

Anticoagulant, to prevent thromboembolism. Platelets may aggregate in the areas of cerebral tissue injury.


CRITICAL TO REMEMBER:

OPIATES (narcotics) and SEDATIVES are contraindicated to the client with increased ICP. These drugs may cause respiratory depression and acidosis.

Care of the client with Seizure Disorder

• Seizure (convulsions) are sudden, excessive, disorderly electrical discharges of the neurons.

• The most common type of generalized seizures are grand mal seizures.

• Grand mal seizures are characterized by aura. Aura may be flashings lights, unusual smells, spots before the eyes, dizziness.

• Tonic-clonic phase of grand mal seizures is characterized by exhaustion, headache, drowsiness, deep sleep of 1 to 2 hours, disorientation.

• The other types of seizures are Petit Mal, Jacksonian seizures, psychomotor seizure, febrile seizures.


• Petiti Mal (“ Absence Seizure or “little Sickness”) is not preceded by an aura. There is little or no tonic-clonic movements. There is sudden cessation of ongoing physical activities. It is characterized by blank facial expression and autmatism like lip-chewing, cheek-smacking. Regain of consciousness is a rapid as it was last; lasts for 10 to 20 seconds. It usually occurs during childhood and adolescence.

• Jacksonian seizures (facial seizures) is common among clients with organic brain lesion like frontal lobe tumor. Aura is present like numbness, tingling, crawling feeling. It is characterized by tonic – clonic movements of group of muscles e.g. hands, foot, or face, then it proceeds to grand mal seizure.


• Psychomotor seizure. It has a psychiatric component. Aura is present (hallucinations or illusions). It is characterized by mental clouding (being out of touch with the environment). The client appears intoxicated. During time of loss of consciousness, there are ongoing physical activities. It is manifested by confusion, amnesia and need to sleep. The client may commit violent or antisocial acts, e.g. Going naked in public, running amok during the time of loss of consciousness.

• Febrile seizures. This is common among children under 5 years of age, when body temperature is rising.


• Status epilepticus. A type of seizure occurring in rapid succession and full consciousness is not regained between seizures. Brain damage may occur secondary to prolonged hypoxia and exhaustion. The client is often in coma for 12 to 24 hours longer, during which time recurring seizures occur. The attack is usually related to failure to take sudden withdrawal of prescribed anticonvulsants.

• Epilepsy. Denotes a group of clinical disorders characterized by the repeated occurrence of any of the various forms of seizures.

Collaborative management for seizure disorders include the following:

1. Stay with the client.2. Protect the client from injury.

Put up-padded side - rails. If the client is sitting or standing, ease him up onto the

floor. Protect head with small pillow or place the head onto the lap.

Do not apply restraints. Do not insert tongue blade. To prevent trauma to gums

and teeth.1. Promote patent airway.

Turn the client to the side. Loosen constricting clothing especially around the neck.


4. Make relevant observation and documentation.

5. Pharmacotherapy: anticonvulsants.

1) Anticonvulsants are classified as follows. Hydantoins Barbiturates Succinimides Oxazolidones/ oxazolidonediones Benzodiazepines Iminostibenes Valproates


2) Anticonvulsant drugs suppress the abnormal electric impulses from the seizure focus to other cortical areas, thus preventing the seizures but eliminating the cause of the seizure.3) Anticonvulsants are classified as central nervous (CNS) depressants.1) HYDANTOINS

Dilantin (Phenytoin) (Mesantoin) Mephenytoin Ethotoin These anticonvulsants have least toxic effects and have small

effect on general sedation and are nonaddicting. The therapeutic serum level of Phenytoin is 10 to 20 mcg./ml. Intravenous infusion of Phenytoin should be administered by

direct injection into a large vein. It should be diluted with normal saline solution. Dextrose solution not be used because of drug precipitate.


Intramascular (IM) injection of phenytoin irritates tissues and may cause damage, therefore this route is discouraged.

Continuous IV infusion of Phenytoin should not be used, because hypotension or cardiac dysrhythmias may occur.

Mephenytoin is more toxic than Phenytoin. This drug is used for severe grand mal or psychomotor seizures that do npot respond to Phenytoin or other anticonvulsant therapy.

Ethotoin produces similar responses as Phenytoin, has a shorter half-life of 3 to 6 hours; therefore, the chance of cumulative drug effects decreases.

Nursing Intervention in Phenytoin Therapy

o Monitor serum drug levels to prevent toxicity.o Ensure adequate nutrition. Phenytoin causes anorexia,

nausea and vomitin.o Initially, avoid driving and performing HAZARDOUS

ACTIVITIES UNTIL THE CLIENT ADAPTS TO DRUG DOSAGE. Drowsiness is apt to occur.

o Avoid alcohol and CNS depressants. These lower seizure threshold.

o To prevent grandmal hyperplasia (overgrowth of gum tissue-reddened gums that bleed easily), advise client to:• Good oral care.• Massage the gums.• Use soft-bristled tootthbrush.• Have preventive dental checkup.

Nursing Intervention in Phenytoin Therapy

o Monitor serum glucose levels of diabetic clients. Phenytoin inhibits insulin release, causing hyperglycemia.

o Monitor complete blood count (cbc). Phenytoin may cause bone marrow depression. Client should report symptoms of sore throat, bruising and nose bleeds.

o Instruct client to take the anticonvulsant at the same time every day with food or milk, to prevent G.I. irritation.

o Phenytoin is contraindicated to pregnancy. It may cause fetal anomalies such as cardiac defects, cleft lip and cleft palate.

The side effects and adverse effects of of HYDANTOINS are as follows:

o Gingival hyperplasia.o Neurologic and psychiatric effects such as ataxia,

nystagmus, sedation, slurred speech, confusion and depression.

o Bone marrow depression- anemia, leukopenia, thrombocytopenia

o Hyperglycemia- the drug inhibits release of insulin.o Gastrointestinal efects: anorexia, nausea, vomiting,

constipationo Drowsiness, headaches, alopecia, hirsutism.o Phenytoin causes pinkish red or reddish-brown

discoloration of urine. This is harmless side effect.

Critical to Remember:

WITHDRAW ANTICONVULSANT DRUGS GRADUALLY TO

PREVENT STATUS EPILEPTICUS.

Anticonvulsants are classified as (CNS) depressants.

2) BARBITURATES Amytal (Ambarbital)-status epilepticus Meberal (Mephobarbital)- grandmal, petit mal Luminal (Phenobarbital)- grandmal, petit mal, status

epilepticus )Mysoline) Primadone- grand mal, psychomotor

seizure Phenobarbital is used to treat grandmal seizures

and acute episodes of status epilepticus seizures. It causes general sedation and drug tolerance.

Discontinue Phenobarbital gradually to avoid recurrence of seizure.


3) SUCCINIMIDES Zarontin (Etosuximide) Celontin (Methsuximide) Milontin (Phensuximide) Used to treat absence or petit mal seizures. Ethosuximide is the drug of choice in this group

of anticonvulsants. Gastric irritation is common; these drugs

should be taken with food.


4) OXAZOLIDONES /OXAZOLIDINEDIONES Paradione (paramethadione) Tridione (Trimetadione) Prescribed to treat petit masl seizures. Withdraw drugs gradually to prevent rebound

seizure.


5) BENZODIAZEPINES The benzodiasepines that have anticonvulsant effects are

as follows:o Klonopin (Clonazepam)o Tranxene (Clorazepate dipotassium)o Valium (Diazepam)o Ativan ( Lorazepam)

Clonazepam is effective in cotrolling petit mal (absence) seizures, myoclonus and status epilepticus.

Chlorazepate dipotassium is administered for treating partial seizures.

Diazepam is prescribed to treat acute status epilepticus. It must be administered IV to achieve the desired response.

Lorazepam is used to control status epilepticus. Infusion rate not exceed 2 mg/min.


6) IMINOSTILBENES Tegretol Carbamazepine) Trileptal (Oxcarbazepine) Carbamazepine is effective in treating

refractory seizure disorders that have not responded to other anticonvulsant therapies. It is used to control grandmal and partial seizures.

Carbamazepine is also used for psychiatric disorders (e.g. bipolar disease), trigimenal neuralgia ( as an analgesic), and alcohol withdrawal.


7) VALPROATE Depakene (Valproic Acid) Depakote (Divalproex Na) Valproic acid is indicated for grand mal, petit

mal and mixed type seizures. Valproic acid is hepatotoxic so liver enzymes

should be monotored. Divalproex Sodium is also used for treatment of

manic episodes associated with bipolar disorder.

Anticonvulsant and Pregnancy

Phneytoin, carbamazepine, trimethadione, valproic acid have tertogenic properties. Valproic acid may cause neural tube deffects (spina bifida).

Anticonvulsant drugs cause loss of folate (folic acid) in pregnant women; thus folate supplements should be taken.

Anticonvulsants tend to act as inhibitors of vitamin k, which contributes to hemorrhaging in infants shortly after birth. Pregnant women taking anticonvulsants are given an oral vitamin k supplement during the last week or 10 days of the pregnancy, or vitamin k is administered to the infant as soon after birth.

Care of the Clients with Altered Level of Consciousness

• Assessment of consciousness includes arousal and content of thoughts.

• Decreased level of cpnsciousness may be due to primary brain injury or disease or systemic conditions like metabolic encephalopathies, hypoxic encephalopathies, toxicity, deficiency conditions.

Collaborative management for altered level of consciousness include the following:

1. Maintain stimulation. Speak to the patient before teaching.2. Maintain nutrition. Administer enteral or parenteral feedings safely.3. Maintain Elimination. Administer stool softeners as ordered.4. Maintain Circulation. Change client’s position at regular basis.5. Maintain normal body temperature.6. Promote safety. Position bed in lowest position and put up padded

side rails.7. Promote activity. Change client’s position, passive ROM exercises.8. Maintain skin integrity. Render hygienic measures, apply lotion, use

protective devices like flotation mattress or air-loss mattress.9. Maintain good hygiene. Render bed bath, hair shampoo, oral care,

nose, ear and eye care, perianal care.10.Support family. Involve family members in the are of the client; help

them explore their concerns, thoughts and feelings.

Care of clients with Headache (Cephalgia)

The different types of headaches are as follows;1. Migraine headache.

Is caused by inflammation and dilatation of blood vessels in the brain. One side of the head is more affected than the other. It tends to occur with stress or life crisis. It lasts for hours or days. The pain is throbbing and pulsatile.

Aura of acute attacks of migraine includes visual field defects, confusion, paresthesia, paralysis in extreme cases.

Associated symptoms of migraine are as follows: nausea and vomiting, chills, fatigue, irritability, sweating, edema, photophobia (sound sensitivity)

Collaborative management for migraine include the following:

Provide quiet, dark environment. Stress therapy and relaxation techniques. Diet: small, frequent meals. Avoid the following foods

chocolate, nuts, onions, food seasoning, cheese, citrus fruits, coffee, pork, dairy products, red wine.

Pharmacotherapy for migraine

1) Beta- adrenergic blockers Inderal (propranolol) Tenormin (Atenolol) Lopressor (Metroprolol)


2) Calcium- channel blockers Calan (Verapamil)

3)Tricyclic antidepressantsElavil (Amitriptyline)Tofranil (Imipramine)

4)Ergotamine tartrate

5)NSAIDsMotrin (Ibuprofen)Naprosyn(Naproxen)


6) Opioid analgesics Demerol (Meperedine) Butorphanol nasal spray

7) Triptans ( Selective Serotonin Receptor Agonists) Imitrex (Sumatripton) Amerge (Naratriptan) Maxalt (Rizatriptan) Zamig (Zalmitriptan)

Triptans cause vasoconstriction, reduce inflammation, and relieve migraine.


Side effects and adverse reactions to lmitrex (Sumatriptan)

o Tingling, nasal discomforto Dizziness, vertigo, drowsinesso Hypertension o Skin rash, swelling of eyelids, lips faceo Nausea and vomitingo Tremorso Wheezing, heart throbbingo Reduced respirationso Seizures, paralysis Lamitrex is contraindicated in hypertension, renal and

hepatic impairment, it should be taken with full glass of water.


2. Cluster headache. Is characterized buy episodes clustered together in quick succession for few days or weeks with remission that lasts for months. The headache is intense, throbbing, deep and often unilateral. It begins in infraorbital region and spread to head and neck.

It is precipitated by alcohol or nitrate. The associated symptoms are flushing, tearing of

eyes, nasal stuffiness, sweating and swelling temporal vessels.

Treatment includes narcotic analgesic during acute phase.


3. Tension headache. Is related to tension and muscle contraction. It is episodic and vary with stress. It is usually bilateral, involves neck and shoulders.

The associated symptoms are sustained contraction of the head and neck muscles.

Treatment includes the following:1) Non narcotic analgesicso Acetaminopheno Propoxypheneo Phenacetino ASA2) Elavil (Amitriptyline)3) Relaxation Techniques

CARE OF THE CLIENT WITH CEREBROVASCULAR ACCIDENT(CVA)

• CVA is caused by disruption of the blood supply to the brain causing neurologic deficit.

• The middle cerebral artery (MCA) is most commonly affected in CVA.

• The second most frequently affected is the internal carotid artery.

• The most common CVA is thrombosis, then followed by embolism, then cerebral hemorrhage.

• CVA due to hemorrhage is associated with activities and occurs during working hours. It is characterized by extensive , permanent loss of function. There is rapid onset of hemephlegia and rapid progression into coma. It is usually fatal.


• Trancient Ischemic Attack (TIA) refer to transient cerebral ichemia with temporary episodes of neurologic dysfunction.

• COMPARISON OF LEFT AND RIGHT CVA

Left CVA Right CVA

• Right hemiplegia • Left Hemiplegia

• Right visual field defect • Left visual field defect

• Aphasia: expressive receptive, global

• Spatial-perceptual field defect

• Altered intellectual activity • Increased distractibility

• Slow, cautious behavior • Impulsive behavior, poor judgment, lack of awareness of deficit


• The clinical manifestations of CVA are as follows: Signs and symptoms of ICP Perceptual defects Aphasia Hemanopsia (Loss of half of the visual field)

• The collaborative management for CVA are as follows: Emergency Care: Care of client with Increased ICP. Care of he client with aphasia.

Promote communication. Practice saying one word at a time. Associate words with objects.


TPN, NGT feeding, gastrostomy feeding. Promote Activity

Turn frequently Perform ROM exercises Prevent contractures.

Promote Elimination Monitor I and O to check for urinary retention Start urinary bowel program


Promote Communication Care of the client with APHASIA

oPractice i=one word at a time.o Identify one object at a time.oGive simple commands.oAnticipate needsoAllow the client to verbalize, no matter how long it

takes him.oReinforce success in speech.oAssist the client in speech therapy.

CARE OF THE CLIENT WITH CEREBROVASCULAR ACCIDENT(CVA) Care of the client with Hemianopsia

Approach the client from the unaffected side of the visual field. Place frequently used articles on the unaffected side of the

visual field. Teach the client scanning technique. Turn the head from side to

side to be able to see the entire visual field. Supportive care:

Promote nutrition (enteral feedings, TPN) Promote activity (Turn frequently, passive ROM exercises). Promote elimination (Monitor I and O, urinary and bowel

program). Provide Emotional Support. Assist in rehabilitation of the client.


Care of the client with Thalmic syndrome: The client experiences emotional lability-

unprovoked crying or crying and laughing at the same time. This behavior is a part of the disease process in CVA. This is due to affection of thalamus that has a center for feelings and the control of emotional expression. The appropriate nursing intervention for the client is provide activities and divert his/ her attention.

CARE OF THE CLIENT WITH INTRACRANIAL TUMORS

• The most common type of brain tumor is glioma. Other types of brain tumor are menigioma, neuroma, hamangioma.

• The clinical manifestations of brain tumor are as follows: Frontal lobe

Personality distrubancesInappropriate affectIndifference of bodily functions

(Precental gyrus-Jacksonian seizures) Temporal lobe

Olfactory, visual or gustatory hallucinationsPsychomotor seizures with automatic behavior

CARE OF THE CLIENT WITH INTRACRANIAL TUMORS

Parietal lobeInability to replicate picturesLoss of right left discrimination

Occipital lobeVisual disturbances preceding convulsions

• Collaborative management for brain tumor include the following:

Care of the client with increased ICP (Preop and post op) Surgery

Supratentotial craniotomyo Place the client in Semi-Fowler’s position.

CARE OF THE CaLIENT WITH INTRACRANIAL TUMORS

Intratentorial craniotomyo Place the client in flat position; turn to sides, avoid

supine position for the first 48 hours. To avoid pressure on the suture line. Avoid neck flexion.

o Report immediately to the physician, yellowish drainage on the head dressing. This indicates CSF leakage.

oMonitor intake and output. Excessive urine output indicates diabetes insipidus. This is due to pressure on the neurophypohysis (posterior pituitary gland).

o Test the urine glucose and acetone when steroids are administered. Steroids stimulate breakdown of fats and proteins. This results to elevation of blood and urine glucose levels and production of ketones.

CARE OF THE CLIENT WITH HEAD TRAUMA

• Head trauma involves injury to the scalp, skull, and or brain tissues.

• Concussion. Is jarring of the brain and against the skull. There is transient period of unconsciousness.

• Contusion. There is bruising or extravasations of blood cells.

• Lacerations. Tearing of tissues caused by a sharp object.

• Compression of the brain. This results from depressed fracture of the skull that causes hemorrhage and edema.


• The clinical manifestations of head trauma are as follows:1) Signs and symptoms of increased ICP.2) Signs of basilar head injury

CSF leaf from ers (otorrhea) and nose( rhinorrhea).

Battle’s sign (Hematoma at the mastoid process/ behind the ear)

NURSE ALERT: BASILAR HEAD INJURYCAUSES COMPRESSION OF THE BRAINSTEM. THE CLIENT MAY HAVE CARDIOPULMONARY ARREST ANYTIME


• Collaborative management for head trauma include the following:

1) Care of the client with increased ICP.

2) Monitor the client for drainage from the ears and nose. Test the fluid for glucose; CSF is positive for glucose).

3) Monitor the client for signs and symptoms of meningitis atelectasis, pneumonia, urinary tract infection.

CARE OF CLIENTS WITH NEUROMASCULAR DISORDERS.

1. Parkinson’s Disease (Paralysis of Agitans)• A degenerative disease that affects the extrapyramidal system

(EPS). This causes decreased dopamine production.• The causes of Parkinson’s diseases are as follows: unknown,

viral infections, drugs, disequilibrium between dopamine and acetylcholine, encephalitis, arteriosclerosis and carbon monoxide poisoning.

• The initial sign tremors –pillrolling tremors, to and fro tremors of the head

• Resting tremors (non-intention tremors). Shaking are more severe when the client is not performing physical activities.

• Rigidity occurs due to decreased dopamine production. Dopamine is a neurotransmitter that promotes muscle relaxation.


• Cogwheel rigidity and absence of arm swing when walking.

• Bradykinesia is slow muscle movement, not associated with muscle weakness.

• Akinesia is absence of muscle movement, not associated with muscle weakness.

• The characteristic gait of the client is shuffling, festinating gait. This is tiptoe walking, starting at a slow pace which keeps on increasing until the client assumes a running pace. The client is unable to stop until obstruction is met.


• The other signs and symptoms of Parkinson’s disease are as follows: Flattened effect (mask-like facial expression) Stooped posture Moist, oily skin (sticky skin) Emotional instability Fatigue Soft, monotonous voice (Microphonia) Shaky, small handwriting(micrographia)• In Parkinson’s disease, there is no intellectual

impairment, no true paralysis, no loss of sensation.


• The collaborative management of Parkinson’s disease are as follows: Thickened liquid diet to soft diet for dysphagia. Firm bed to prevent contractures. Aspiration precaution Increase fluid intake and fiber in the diet to prevent constipation Pharmacotherapy

Antichollinergics. Reduce the rigidity and some of the tremors in Parkinson’s disease. Artane (Trihexyphenidyl) Cogentin (Benstropine) Akineton (Biperiden) Kemadrin (Procyclidine) Parsidol Ethopropazine) Norflex (Orphenadrine)

CARE OF CLIENTS WITH NEUROMASCULAR DISORDERS.• Nursing Interventions for Anticholinergics

1) Monitor VS, urine output, and towel sounds. Increased pulse rate, urinary retention and constipation are side effects of anticholinergics.2) Observe the client for involuntary movements3) Advice to avoid alcohol, cigarette, caffeine and aspirin to decrease gastric motility.4) Prevent and relieve side effects of anticholinergic decrease salivation.

o Relieve dry mouth with hard candy, ice chips or sugarless chewing gum. Anticholinergics decrease salivation.

o Suggest that the client use sunglasses in direct sun because of possible photophobia.

o Advise the client to void before taking the drug to minimize urinary retention.

o Advise the client to have routine eye examinations to determine the presence of increased intraocular pressure which indicates glaucoma. Clients who have glaucoma should not take anticholinergics.


Dopaminergics. These drugs improve muscle flexibility. Levedopa Carbidopa with levodopa (Sinemet). Dopamine cannot cross blood-brain barrier. Levodopa, a precusror of dopamine can cross the

blood-brain barrier.


The enzyme dopa decarboxylase converts levadopa to dopamine in brain. However, this enzyme is also found in the peripheral nervous system, thereby allowing 99% of levodopa to be converted to dopamine before it reaches the brain (1% reaches the brain). Therefore, a higher dose is required to achieve therapeutic effect of the drug. Because of high doses, many , side effects occur including nausea, vomiting, dyskenesia, orthostatic hypotension, cardiac dysrhythmias nand psychosis.

Carbidopa and levodopa (Sinemet). Carbidopa reduces destruction of levedopa at the periphery. A single dose per day is administered.


Nursing Interventions in Carbidopa-Levodopa therapy

1) Monitor the client’s vital signs and ECG. Orthostatic hypotension may occur.

2) Check weakness, dizziness or syncope, which indicate orthostatic hypotension.

3) Advise client to practice gradual change in position to prevent orthostatic hypotension.

4) Inform the client that urine may discolor and will darken (reddish brown) with exposure to air. Perspiration may also be discolored. Both are harmless but clothes may be stained .


5) Symptoms of dyskinesia (impaired voluntary movement) may take weeks or months to be controlled.

6) Advise client to avoid the following drugs:a. Phenothiazines, pyridoxine (Vit. B6). Reserpine.

These Block the effect of Levedovapa.b. Monoamine oxidase inhibitors (MOAI)

o Marplan (Isocarboxacid)o Parnate (Tranyclypromine)o Nardil (Phenelzine)


MAOIs enhance norepinephrine activity.MAOis + Carbidopa w/ Levedo= Hypertensive crisis

c. Aldomet (Methyldopa). This potentiates effect 7) Avoid the following foods when on Carbidopa- Levodopa

therapy:a. Vitamins B6- rich foods like tuna, pork, dried

beans, salmon, beef liver,. These foods block effects of levodopa.

b. Tyramine- rich foods. These foods may cause hypertensive crisis among clients on Levodopa therapy.

o Cheezeo Cream


o Yogurto Coffeeo Chocolateo Bananaso Raisinso Italian green beanso Livero Pickled herringo Sausageo Soy sauceo Yeasto Beero Redwine(These foods are proteins, aged, smoked and fermented)


8) Prevent and relieve the following side effects of Levodopa. Nausea and vomiting Hypertension, Orthostatic hyppotension Insomnia, Agitation Mental confusion Renal damage

Dopamine Agonists/ Antiviral Drugs. These medications act on the dopamine recpetors and produce improvement in symptoms of Parkinsonism.

Symmetrel (Amantadine HCL) Parlodel ( Bromocriptine Mesylate) Requip (Ropinozole HCL)


Nursing Intervention in Dopamine agonists therapy

1) Advise the client to report signs of skin lesions, seizures or depression (Amantadine).

2) Suggest to the client to report lightheadedness when chaning positions (Bromocriptine)

3) Avoid alcohol.

4) Advise client not to abruptly stop the drug without notifying the health care provider.

CARE OF CLIENTS WITH NEUROMASCULAR DISORDERS

Other drugs for Parkinson’s disease Monoamine oxydase- B inhibotor. It inhibits

breakdown of Dopamine, thus prolonging action of Levodopa.o Tasmar (Tolcapone)o Comtan (Entacapone)


2. MYASTHENIA GRAVIS (MG)• Is a neuromascular disorder characterized by failure of

transmission of nerve impulses at the myoneural junction.

• MG may be caused by decreased number of functioning acetylcholine receptors sites. It is also associated with autoimmune disorders.

• DECENDING MUSCLE WEAKNESS• INCIDENCE RATE: Women aged 20-40 years old• The clinical manifestations of MG are as follows: Muscle weakness associated with activity relieved by

rest, e.g. dyspnea, dysphagia, decreased physical activity. Fatigue


Ptosis, diplopia, strabismusImpaired speechSnarl smile, masklike facial expressionDysphagia, droolingRespiratory difficulty

PTOSIS DIPLOPIA STRABISMUS


• The diagnostic test for MG is Tensilon Test (Edrophonium) test

• Tensilon test a short-acting cholinergicas

• Tensilon is administered IV (2mg. First, then 8 mg.). Positive Tensilon Test is observed as improvement in mascular strength. Muscles weakness returns in 3 to 5 minutes.

• The antidote for cholinergic is Atrophne sulfate (anticholinergic).

• Tensilon is not used as a treatment for MG since it is short acting, and has no sustained therapeutic effect.

• The client should not be informed that the medication is given to obtain true results.


• Collaborative management for MG are as follows:Assess swallowing and gag reflex before feeding the

and client. To prevent aspiration.Administer medications 20- 30 minutes before

meals. To improve ability to swallow and to prevent choking.

Administer medication at exact time. To prevent myesthenia crisis that results to respiratory distress.

Protect the client from falls due to muscle weakness. Implement aspiration precaution.Start meal with cold beverage. To contract muscles

of the throat and improve ability to swallow.


Promote adequate ventilation. To relive respiratory difficulty.

Avoid infections. Infections may trigger excacerbations of MG.

Provide adequate rest with alternating activity.Plasmapheresis. This involves separation of

antibodies from the plasma to inhibit autoimmune response.


Pharmocotherapy for MG

1. Acetylcholinesterase inhibitors/Cholinesterase inhibitors Prostigmin (Neostigmine) Mestinon (Pyridostigmine) Mytelase (Ambenomium) These medications transmits neuromuscular

impulses by prevening the destruction of acetycholine. Therefore, there is increased muscle strength.


Nursing interventions for Acetycholinesterase Inhibitorsa) Monitor improvement of muscle strength and

respirations.b) Observe the cliet for signs and symptoms of

cholinergic crisis caused by overdosing of the drugs, eg., ,uscle weakness, increased salivation, sweating, tearing and miosis.

c) Have a readily available antidote for cholinergic crsisis(Atrophine sulfate).

d) Encourage the client to take medications before meals for best drug absorption.


f) Observe and report possible side effects and adverse reactions (cholinergic reaction): Nausea, vomiting, diarrhea, abdominal cramps Increased salivation Tearing Miosis (constriction of pupils) Possible hypertension

2.Glucocorticoids. For anti-inflammatroy effects.

3.Antacids. To prevent gastrointestinal upset due to glucocorticoids.


• Surgery: Thymectomy (surgical removal of the thymus gland). Twenty Five percent( 25%) of people with MG have been found to have thymoma (tumor of the thymus glands). This surgery achieves remission (symptom-free) for 5 to 10 years.

• The 2major complications of MG are myesthenia crisis and cholinergic crisis.

• Myastheni crisis is caused by undermedication.


• The clinical manifestations of myesthenia crisis are as follows.o Sudden marked rise in BP due to hypoxia.o Increased heart rate.o Severe respiratory distress and cyanosis.o Absent cough and swallow reflex.o Increased secretions, increases diaphoresis and

increased lacrimation.o Restlessness, dysarthriao Bowel and bladder incontinence.


Interventions for myasthenic crisis are as follows:Increase doses of cholinergics as long as the client

responds positively to Endrophonium treatment.Possible mechanical ventilation if respiratory

muscle paralysis is acute.Cholinergic crisis is causd by excexssive medications.The clinical manifestations of cholinergic crisis are as

follows:oWeakness with difficulty swallowing, chewing,

speaking and breathing.oApprehension, nausea and vomiting.


oAbdominal cramps and diarrheao Increased salivation and secretions.oSweating, lacrimation, fasciculation (muscle

twitch), and blurred vision. Interventions for cholinergic crisis are as follows:

oDiscontinue all cholinergic drugs until cholinergic effects decreases.

oProvide adequate ventilators support.o1 mg. IV atropine may be necessary to counteract

severe cholinergic reactions.


The following drugs should be avoided by the client with MG:Muscle relaxantsBarbituratesMorphine sulfateTranquilizersNeomycin

These drugs potentiate muscle weakness because of effect on myoneural junction.

CARE OF CLIENTS WITH NEUROMASCULAR DISORDERS• Survival Guide for clients with MG

Reschedule daily tasks. To prevent weakness. Secure “handicapped” parking sticker. Frequent rest periods. Have alarm clock available- to take medications on time.

This prevents myasthenic crisis. Patch each eye alternately for diplopia (double vision). Start the meal with cold beverage. To conduct constriction

of muscles of the throat and prevent aspiration. Avoid factors that affect respiratory infections:

Very hot or very cold weather.Aerosol, pesticides , cleaners.Alcohol, tonic water, cigarette smoke.


• Multiple Sclerosis (MS) Is an autoimmune disorder that causes destruction of

myelin sheath of nerve fibers in the brain and spinal cord (CNS).

It is characterized by remissions and exacerbations.There is elevated 1g /G in the CSF.Evoked potentials show slowed nerve conduction.MRI of the brain and spinal cord shows presence of

MS plaques.Shawann’s cells of the myelin sheath are destroyed.

This results to interruption and distortion of impulse (slowed or blocked).


The clinical manifestations of MS are as follows:Eye manifestations (optic nerve involvement)- vision

lossWeakness or tingling sensation (paresthesia due to

involvement of the cerebrum and soinal cord).Incoordination due to cerebellar involvement (ataxic

gait).Bowel and bladder dysfunction as a result of spinal

cord invovlement.Muscle fatigue due to muscle spasticity.Charcoat’s Triad:

S – canning speech I – ntention tremors N – ystagmus


Exacerbations may be aggravated by fatigue, chilling and emotional stress.

The collaborative management for MS are as follows:Patch the eye alternately for diplopia. Provide well-balanced diet, high in fiber to prevent

constipation.Physical therapy to improve muscle strength and to

avoid contracture.Avoid hot baths. Heat Increases weakness.Force fluids to prevent constipation and infection.Speech therapy to relieve scanning speech.Plasmapheresis. To inhibit autoimmune response.


Pharmacotherapy in MS1. Glucocorticoids

Prednisone Decadron (Dexamethasone) Corticotropin

2. Muscle Relaxants. To relieve muscle spasm. Lioresal (Baclofen) Betaseron (an interferon that reduces spacticity)

3. Immunosuppressants. To reduce relapse of MS. Imuran (Azathiorpine) Cytoxan (Cyoclophosphamide)


• ALZHEIMER’S DISEASE Is a degenerative disorder of the cerebral cortex

resulting to microscopic plaques. It is characterized by impaired intellectual function

and progressive loss of ability to carry out activities of daily living.

Loss of recent memory occurs first. Remote memory may remain intact for long period of time.

The cause of Alzheimer’s disease is unknown but it may be associated with autoimmune disorders and heredity.


The stages and phases are as follows:

Stage 1. Mild (Early confusion).Early cognitive decline in one or more areas,

memoryloss, decreased ability to function in work situation, name- finding deficit, same decrease in social functioning, recall difficulties, anxiety.

Stage 2. ModerateUnable to perform complex tasks such as managing

personal finances or planning a dinner party, unable to concentrate; no knowledge of current events.


Stage 3. Moderately severe (Early dementia) Usually needs assistance for survival; needs reminders to

bathe, help in selecting clothes and other daily functions, maybe disoriented as to time and recent events although this can fluctuate, may become tearful.

Stage 4. Severe (Demetia) Needs assistance with dressing, bathing and toilet

functions (flushing); may forget spouse, family and caregiver’s names, details of their personal life; generally unaware of their surroundings, incontinence of urine and feces; increase in central nervous system disturbances such as agitation, delusions, paranoia, obsessive anxiety, increased potential for violent behavior and tendency to wander.


Stage 5. Very severe (Late Dementia) Unable to speak (speech limited to five words or less), person

may scream or make other sounds, unable to ambulate, sit up, smile , or feed self; unable to hold head erect; will ultimately slip into stupor or coma.

• The collaborative management for Alzheimer’s disease: Protect the client form injury. The client has tendency to wander

around. Provide close supervision. Close and secure doors. Use ID bracelets and electronic surveillance. Remove throw rugs, toxic substances and dangerous electrical

appliances from the environment. Reduce hot water heater temperature. Orient client to the environment.


Promote activity.Provide exercise such as walking with an escort.Provide activity that distract and and occupy time

such as listening to music, coloring, and watching television.

Provide mental stimulation with simple games and activities.

Promote activities of daily living.


Promote sleep Allow client to wander in a safe place until he or she

becomes tired.Prevent shadows in the room.Avoid the use of hypnotics because they cause

confusion and aggravate the sundown effect. Avoid Agitation and Violence

Assess and remove the cause of agitation.Avoid scolding, embarrassing, arguing or reasoning

with the client.Approach the client slowly and calmly.Remove the client from stressful environment.


Minimize confusion and disorientationCall the client by name.Orient the client frequentlyAsk only one question at a time and give one direction

at a time.Use familiar objects in the room.Place a calendar and clock in a visible place.Provide structured activities (routine schedule).Allow the client to reminisce (remote memory may

remain intact for a long time).Provide simple environment that requires less decision

making.Allow time for the client to complete task.


Prevent fatigue by avoiding the following:Change of routineExcessive demandsPhysical stressorsOverwhelming situation.

These factors escalate behavioral dysfunction.Prevent sundown syndrome.

Turn lights on before it becomes dark.Refer Family to support groups: The Alzheimer’s

Disease and related disorders.


Tacrine May improve cognitive functions for mild to

moderate Alzheimer’s disease.Check VS periodically, for tachycardia and

hypotension.Exelon

G.I. upset common adverse effect. Weight loss may be a problem.


Amyotrophic Lateral Sclerosis (ALS)

• Is a progressive degenerative disease involving the motor system.

• It is also called Lou Gehrig’s Disease.• The cause of the disease may be related to an excess of

glutamate, a chemical responsible for relaying messages between motor neurons.

• The clinical manifestations of ALS are as follows:Fatigue and weakness while talking.Awkwardness of fine finger movements.Dysphagia (1st sign)Muscle weakness and atrophy


Muscle wasting Unilateral disability of arm and leg. Dysarthia Fasciculation of the face. Jaw clonus Respiratory difficulty

• Collaborative management for ALS care as follows: Supportive and symptomatic Monitor and promote respiratory function. Gastrostomy feeding Avoid aspiration Assist with ADL Provide emotional support to the client and family.


Guillan –Barre Syndrome (GBS)

• Is an acute infections neuronitis of the cranial and peripheral nerves.

• It involves destruction of the myelin sheath due to autoimmune disorder.

• It may follow swine flu vaccine.• It is usually preceded by mild upper respiratory

infection or gastroenteritis.

• The recovery is slow process.

• The main problem is difficulty of breathing.


The clinical manifestations of GBS are as follows: Ascending or descending paralysis which may progress to

respiratory muscle paralysis. Tingling and numbness. Cardiac dysrhythmias. Elevated protein levelin CSF. Abnormal EEG (electro encephalography)Collaborative management for GBS are as follows: Symptomatic and supportive. Monitor and promote respiratory function. Prevent complications of immobility. Monitor cardiac status.


Trigeminal Neuralgia (Tic Douloreux)• A sensory disorder of the fifth cranial nerve.• It is a manifested by excruciating, recurrent paroxysms of

sharp, stabbing facial pain along the trigeminal nerve (lips, gums, nose, cheeks)

• Pain aggravated by cold, washing the face, chewing, hot or cold foods and fluids, touch of wind on the face.

Collaborative management for Trigeminal Neuralgia are as follows:

Instruct the client to avoid hot or cold foods and beverages.

Provide liquid and soft foods. Instruct client to chew food on the unaffected side.


PharmacotherapyElavil (Amitriptyline)Lioresal (Baclofen)Tegretol (Carbamazepine)Valium (Diazepam)Dilantin (Phenetoin)


Bell’s Palsy (Facial paralysis)• Is caused by lower motor neuron lesion of the seventh cranial

nerve.• It may be caused by infection, trauma, hemorrhage,

meningitis or tumor.• It is manifested by paralysis of one side of the face with

drooping of the eyelids, or puff out the cheeks.Collaborative Management for Bell’s palsy are as follows: Encourage facial exercises. Protect the eyes from dryness and prevent injury. Promote frequent oral care. Instruct the client to chew on the unaffected side.


PharmacotherapySteroidsAnalgesic


Care of the Client’s with Spinal Cord injury (SCI) Spinal cord injury occurs in the following situations:

Falls, Diving, Vehicular accident. SCI results to the following effects below level of the

lesion:ParalysisLoss of reflexesLoss of sensory functionLoss of motor functionAutonomic dysfunction


Clinical manifestations of spinal cord injury

1) Cervical SCI

Injuries at C2 and C3 are usually fatal.

Quadriplegia (paralysis of our four extremities) Respiratory muscle paralysis. Bowel and bladder retention.

2) Thoracic SCI Paraplegia (paralysis involving the lower extremities). Poor control of upper trunk. Bowel/ bladder retention.

Autonomic dysreflexia with lesion or injury above T6


3) Lumbar SCI Paraplegia (Flaccid paralysis) Bowel and bladder retention.

4) Sacral SCI Injury above S2 in males allow erection but there

is no ejaculation. Injury between S2 to S4 prevents erection and

ejaculation. Paraplegia Bowel and bladder incontinence.


The higher the level of lesion, the greater is the probability to perform sexually.

The lower the level of lesion, the lesser is the probability to perform sexually.

The paraplegic male may experience impotence. The paraplegic female is capable of pregnancy, but

is unable to experience orgasm.Collaborative management for SCI are as follows: First priority: promotion of respiratory function

especially in cervical SCI. Immobilize in a flat, firm surface. To prevent further

injury.


Apply cervical collar especially if cervical injury is suspected.

Transport client as a unit. Do not attempt to realign body parts. Definitive management.

1) Traction2) Cast3) Surgery

Monitor and manage potential complications of SCI1) Spinal Shock (neural sock, areflexia). It is a period of flaccid paralysis and a complete loss of all reflexes occurs.


The clinical manifestations of spinal shock are as follows:o Absence of sweating below the level of the

lesion.o Bowel and bladder retention.


o Hypotension, Bradycardia If the lumbosacral segment are undamaged, spinal

shock wears off in 2 to 3 weeks The first sign of resolution of spinal shock is

contraction of the quadriceps (Hamstring) muscles and flexion or extension of toes on plantar stimulation.

The other signs of resolution of spinal shock are reflexive emptying of the bladder, reflex defecation and return of sweating.

2) Autonomic Hyperreflexia (dysreflexia). It occurs in clients with SCI above T6; most often cervical injuries.

It causes hyperstimulation of symathethic nervous system (SNS).


It is caused by visceral distention like bladder distention, fecal impaction and skin stimulation like pressure sore below the level of lesion.

The clinical manifestations of autonomic hyperflexia are as follows:o Severe headacheo Blurring of visiono Nasal congestiono Nausea and vomitingo Hypertension, bradycardiao Sweating above the lesion; pilomotor spasm (goose

flesh) below the lesion. The most dangerous effect of autonomic dysreflexia is severe

hypertension. This may lead to blindness and CVA.


Collaborative management for autonomic dysreflexia include the following:o Place the client in sitting position. To lower BP

by gravity.o Check bladder distention. Catheterize client as

indicated.o Check fecal impaction. Perform manual extraction

as indicated.o Turn the client to sides at regular intervals. To

prevent pressure sores.o Pahrmacotherapy:

• Hexamethonium Chloride (a ganglonic b;ocking agent)

• Nitroprusside ( a vasodilator)


Whiplash injury Is caused by violent hyoerextension and flexion of the

neck. It usually result from vehicular accident. There is damaged to muscles, disks, ligaments and

nervous tissues of the cervical spine. The clinical manifestations of whiplash injury are as

follows: Pallor Weakness Gait disturbance Dizziness Nausea and vomiting Occipital headache Nuchal rigidity


Collaborative management for whiplash injury include

the following: Promote bed rest. Apply cervical collar as needed. Apply hot packs to the neck as indicated. Administer analgesic and muscle relaxant as

prescribed.

MENINGITIS

- inflammation of the meninges of the brain and spinal cord.

ETIOLOGIC AGENTS• MENINGOCOCCUS – MOST DANGEROUS• Pneumococcus• Streptococcus – adult• Hemophilus influenzae – pedia

MODE OF TRANSMISSION – airborne transmission via droplet infection

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Signs & Symptoms

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DIAGNOSTICS

meningitis

CSF analysis will reveal

• Increased CHON and WBC• Decreased Glucose• Increased CSF opening pressure

• N = 50-160 mmHg

• (+) cultured microorganisms

• These confirm presence of meningitis

NURSING MANAGEMENT

1. Complete bed rest

2. Administer medications as ordered

- Broad Spectrum Antibiotics

- Penicillin

- Analgesics

- Antipyretics

3. Institute strict respiratory isolation after initiation of antibiotic therapy

4. Institute ICP monitoring

5. Dim environment d/t photophobia

neurological disorders

Health & Medicine