curative and rehabilitative ncm of client with neurologic disorders

8/4/2019 Curative and Rehabilitative NCM of Client With Neurologic Disorders

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Neuro Nursing Ms. Jean Javier

1

Curative and Rehabilitative NCM of Client with Neurologic Disorders

Overview of the anatomy and physiology of the nervous system

1. Supporting Structuresa. Skullb. Meningesc. CSFd. Blood Brain Barriere. Blood Supply

2. CNSa. Brainb. Spinal Cord

3. PNSa. Cranial nervesb. Spinal nerves

o Somatico Autonomic

Sympathetic Parasympathetic

Neurologic Disorders

1. Seizure Disorders2. MS3. MG (Acetylcholine is affected in this disease)4. Parkinsons disease (Paralysis agitans)5. CVA stroke or brain attack; altered blood supply to the brain6. Alzheimers Disease lack of neurotransmitters and the role of toxic Al7. Headache attention headache or muscular headache or migraine headache8. Head Injury9. Spinal Cord Injury (SCI)

Outline Per Disorder

o Definitiono Nursing assessmento S/Sxo Lab dxo Med mgto N mgto NCPo Case analysis

Diagnostic Studies

1. Skull and Spinal radiography


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2. Computed tomography scan3. MRI4. Lumbar Puncture5. Myelogram6. Cerebral Angiography7. EEG8. Caloric testing

Overview of the Grading System

Q 50%

TE 40%

Other Req 10% (Updates and Readings)

Anatomy of the Brain and the Spinal cord

Nervous System should be well shielded

Principle

1. Should be well shielded and hierarchy of control protected because it is the brain that controls uppercenters

2. Specialized tissues less able to survive when there is problem or deficit such as less oxygenation; braincells does not regenerate

3. When there is a destruction those remaining are unable to replace those that are lostEg. CVA if there is problem in the left side, affectation in the right side

Left side verbal and analytical skills

4. Hierarchy of control, higher center will control the lower centers there is always a collaboration, no partcan function independently

5. The nervous system imposes regulation and control not only to an organ or system but also in itself

Sensory impulses Receives, transmits, computes, integrate, responses are sent to the motor or efferent/effector

nerve tract

A. Supporting Structures1. Skull/Cranium

- Bony helmets (composed of bones)- Collection of 22 bones (8 cranial bones and 14 facial bones)

Frontal - 1

Temporal 2

Parietal - 2

Occipital - 1

Sphenoid - 1forms the orbits, looks like a butterfly


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Ethmoid - 1

- 14 cranial bonesMaxillae - 2

Zygomatic -2

Nasal bone -2

Lacrimal bones -2

Palatine bones -2

Inferior nasal conchae - 2

Vomer -1

Mandible -1

- Rigid chamber with opening at the base (foramen magnum)- Bones are not fused until 18th months- Infants skull is not a rigid structure- 6 fontanels only 2 are palpable anteriorlateral 2, posteriorlateral 2; 1 anterior 1

posterior fontanel

- Fontanelsi.

Anterior fontanel 9-18 monthsii. Posterior fontanel 2-3monts

- Head circumference is usually 1.25-2.5cm larger than the chest circumference; if the headsize is equal to the chest circumference the head is small (microcephaly); if the head size is

4 cm larger than chest circumference microcephaly/hydrocephalus refer to the staff nurse

then to MD for further assessment and observation

2. Meninges- Surrounds and protects the brain and spinal cord- Provides nourishment to the brain and the spinal cord- Found in the skull and the spinal canal

a. Dura Mater Thick and durable; gray in color Vascular there are venous channels, venous sinuses (accounts for greyish

color) found in the Dura matter where the CSF in dumped inelastic

Cloaklike Venous sinuses

b. Arachnoid Mater Thin and delicate Lies between the dura and pia Avascularcomposed of tiny blood vessels Colored white Web like structures thin Elastic Has arachnoid villi finger like structures that are found to be absorbing

the CSF; great role in the problem of hydrocephalus (communicating types

of Hydroceph)

c. Pia Mater Below the arachnoid


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Hugs the brain follows every convolution Vascular No space between pia and brainGyrus/gyrielevated, coil

Sulcus/sulcus shallow/depression

- 3 Potential Spaces Within the Structures of Meninges1. Epidural Space

- bundle of nerves ; lots of BV crossing the epidural space; epidural hematoma canoccur fast if there is an injury

- external to dura2. Subdural Space between Dura and arachnoid; hematoma can occur3. Subarachnoid Space between arachnoid and pia; potential space where CSF

circulates under N conditions

3. CSF- Clear, colorless fluid- Protective cushion that supports the brain- Nourishment glucose and O2, lymphocytes- Secreted from the choroid plexus that supports the brain little clusters that looks like

raspberries; found in the walls of our ventricles; produces CSF in greater amounts (2/3)

- Normal pressure : 100-180mmHg- Ependymal Cell with cilia which cause movement of the CSF, produces lesser amount of CSF

(1/3)

- CSF is produced at the rate of 18mL per hour or approx 500-700cc/day approx 100-160 mis circulated in Subarachnoid space

-

only a little amount is retained in the circulation particularly in the ventricular system(ventricles) 12-15mL it may cause hydroceph if more

- Ventricles left and right lateral ventriclesRLV LLV

Right cerebral hemisphere Left Cerebral hemisphere

- There is a foramen in between known as Foramen of Monro; aka InterventricularForamina going to

- 3rd Ventricle (slit like space between the thalamus) produces its own CSF Aqueduct of Sylvius going to

- 4th Ventricle (located between the pons and the cerebellum)-

3 openings in the roof of the 4

th

ventricle- Has 3 openings; 2 (Left and Right) Foramen of Luschka going to the Subarachnoid space in

the brain where there is arachnoid villi that absorb CSF and dumps it to venous sinuses

then down to jugular vein to the superior vena cava;

- 3rd opening aka Foramen of Magendie leading to the posterior spinal canal to the sidesand then to the anterior to the SA space in the brain where it will be absorbed in the

Arachnoid Villi the get and dumped in the venous sinus to the systemic circulation

- Astrocyte very important when we talk about blood brain barrier


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Arnold Chiari Malformation malformation of the cerebellum and the medulla oblongata;

there is caudal displacement of the medulla oblongata, the medulla will be pushed to the

cerebellum obstructing the flow of CSG non communicating Hydrocephalus

- Monro-Kellie principle inc in any one of the 3 components can cause an increase in ICP i. Bain tissue N is- 88%ii. CSF 8-9%;

iii. Intravascular blood 2-3%- 4-15mmHg N ICP

4. Blood Brain Barrier and Blood Supply- Filter/brain parenchyma that protects the CNS from being affected by many potentially

harmful agents

- Least semi-permeable membrane- Semi-permeable capillaries which separates parenchyma of the CNS from the blood- Astrocytes and Pia matter allows passage of small particles nutrients, O2, CO2, essentia

amino acids, glucose, lipids

- It does not allow non essential amino acids, metabolic wastes materials, urates/uric acid,toxins, some microorganism allows this to pass through if there is aninjury/alteration/nutrients

- Useless against fat soluble materials/molecules May cause CVA Fat soluble nicotine, alcohol (frontal lobe is affected motor affectation) and

anesthesia (GA)

- Endothelial cells-Astrocytes-CSF barrier, passes O2 glucose, essential amino acids, allowsthis to go out of the blood vessels

Blood Supply

- Caries O2, nutrients, and waste materials- 2 main parts of artery supply

2 internal carotid arteries ACerebralA anterior MCerebralA lateral portion of the brain

2 vertebral arteriesThe internal carotid arteries supply the frontal area

Cerebral arteries are connected by communicating

arteries forming an arterial circle at the base of the

brain known as the Circle of Willis


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Central Nervous System (Brain-Spinal Cord)

Brain

Protection: Skill

Nerves: Cranial 12

Motor: 5

Sense: 3

Moto/Sense: 4

Spinal Cord

Location No. of Pairs

Cervical 8

Thoracic 12

Lumbar 5

Saccral 5

Coccyx 1

4 Parts of the Brain

N Weight 1.4 Kg 3 lbs.

a. Cerebrum- Consists of 4 lobes: frontal, parietal, temporal, occipital

1. Frontal: motor, motor speech, controls, morals, values, emotions and judgment, inhibition andaffection

- Concentration, abstract thought, information storage and memoryBrocas Area left side motor speech (word formation) resulting to slurred speechExpressive Aphasia

2. Parietal Lobe sensory lobe integrates general sensation, interprets pain, touch, temperature,pressures and governs discrimination

3. Temporal Lobe- auditory receptive area, sensory speech- Contains interpretative area that provides integration of somatisation, visual and auditory areas

Wernickes Area posterior part of the superior temporal convulsion to the posterior lobe

- Could not understand spoken words- Receptive Aphasia

*** Wernickes andBrocas are affectedGlobal Aphasia may result d/t CVA or any injury

4. Occipital Lobe visual areab. Cerebellum

- Balance/equilibrium, muscle tension, spinal nerve reflexes, coordination- Hind Brain

c. Diencephalon- Composed of 2


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- Structures: Thalamus/Hypothalamus- Thalamus contains the 3rd ventricle

Thalamus screens and relays sensory impulses to the cortex More important impulses are sent to the brain and responded upon

- Hypothalamus Regulates ANS Stress response Temperature regulation Affects emotion Fluid balance Hunger Sexual desires Sleep pattern

d. Brain Stem- Midbrain, pons, Medulla oblongata- Midbrain

Conjugate eye movement (simultaneous movement of eyes including pupil reactions)

Motor coordination- Pons

Involuntary respiratory reflexes, breathing pattern- Medulla Oblongata

Vomiting center Vehicular accident/neck area Cardiac, Respi, Vasomotor center Decussations of nerve tracks and neurons occur greater of percentage of crossing over of

nerve tracks and neuron

***Spinal Cord from the medulla oblongata passes through foramen magnum

***SC ends in approx L2

White matter myelinated

Posterior horn cell Dorsal receives sensory or afferent impulses from the dorsal root

Anterior horn cell Ventral sends efferent or motor impulses to the ventral root

***Spinal reflex arch

***Substantia gelatinosa responsible for opening pain impulses acts as a gate for what impulses to be allowed

Peripheral Nervous System

Somatic Nervous System

- Reacts to outside stimuli- Receiving of sensory impulses from external environment- Conscious control


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- Innervates our striated muscles/voluntary- Located in the skin

Autonomic Nervous System

- Maintains homeostasis- Unconscious control- Innervate involuntary functions of the bodyo Sympathetic

- Origin: Thoracic/Lumbar- Response: Involuntary- Fight or Flight Response- Sympathetic = ThoracolumbarT1-L2 ~ Adrenergic System ~ Catabolic- E Division emergency, excitement, exercise, embarrassment- Increase everything except GIT, GUT- Vasoconstriction ~ increase BP- Bronchodilation- Pre ganglionic shorter as compared to the post ganglionic Acetylcholine- Post ganglionic synapse Norepinephrine, Noradrenalin-

o Parasympathetic- Origin: Brain/Sacral- PCCraniosacral Division- Cholinergic~ Anabolic- D Division Digestion, Diuresis, Defecation- Response: Normal- Decrease everything except GIT, GUT- Vasodilation, Bronchoconstriction- Acetylcholine

Cranial Nerves

1. Olfactory S (Olfactory Bulb)2. Optic S (Thalamus)3. Oculomotor M (Midbrain)4. Trochlear M (Midbrain)5. Trigeminal SM (Pons)6. Abducens M (Pons)7. Facial SM (Pons)8. Acoustic/Auditory/Vestibulocochlear S (Pons)9. Glossopharyngeal SM (Medulla oblongata)10.Vagus SM (Medulla oblongata)11.Accessory M (Medulla oblongata)12.Hypoglossal M (Medulla oblongata)


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Spinal Nerves

Cervical 1-8

Thoracic 1-12

Lumbar 1-5

Saccral 1-5

Coccygeal 1

31

C1-C7-exit above corresponding vertebra

***C8-below C7 and above T1

T1-Coccygealbelow corresponding vertebra

Cauda equina bundles of nerves, like a horse tail

Seizure Disorders

-

Convulsion, attacks or fits- Episodes of abnormal motor sensory, autonomic or psychic activity resulting from sudden excessive

discharge of electrical activity of the

- Abruptness or spasm like character of an event- Excessive cortical discharge- Neuronal discharge rate can reach 1000firing/sec sudden or excessive

Firing depends on the waveConvulsion abrupt violent contraction of muscle; this is just part of the seizure

Epilepsy

- Sudden, transient alterations of brain function- Recurrent episodes of paroxysmal neurologic function manifested by loss of consciousness, convulsivemovements and behavioral abnormalities

- Chronic recurrent disorders- Recurrent seizures- A single seizure cannot contribute to an epileptic attacktake note of the clients history

Status Epilepticus

- Consist of a train of severe seizure with relatively short intervals or not intervals between one seizure toanother

- Continuous- Can endanger life of the patient

***Patient becomes fatigued, bronchoconstriction causing hypoxia or anoxia

Categories of Seizures

1. Generalized seizure may involve both cerebral hemisphere and entire cortical surface1. Tonic-Clonic (Grand Mal)

Last for 2-5 min


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Consciousness is lost suddenly and seizure follows Aura may or may not be present (warning of impending seizure)

Tonic Phase- stiffening or rigidity of the muscles particularly of the arms and legs- Immediate loss of consciousness; arching of the body, eyes are wide open- Locked or fixed jaw- A cry may be uttered when the seizure starts- Respiration is interrupted temporarily and may become cyanotic- The jaws fixed. Hands clenched. Eyes wide open. Pupils dilated and fixed- Lasts for 30-60***Epileptic Cryis caused when air passes through the larynx that is partially closed by a

spastic glottis

Clonic Phase- Rhythmic jerking of all extremities incontinent of urine or feces- May bit lips, tongue or insides of mouth- Respiration will be a little bit noisy or stertorous because of froths in the mouth of the

patient2. Absence (Petit Mal)

Brief period of decreased responsiveness or cessation of ongoing activity Occurs suddenly without warning and ends suddenly Temporarily stopped doing activity

3. Tonic Seizure Characterized by an abrupt increase in muscle tone, loss of consciousness and loss of autonomic

signs lasting from 30 seconds to several minutes

4. Clonic Seizure Last several minutes and is characterized by muscle contraction and relaxation

5. Myoclonic Seizure Characterized by a brief jerking or stiffening of the extremities which may occur singly or in groups Lasts for just a few seconds, the contraction may be symmetric or asymmetric Brief shock like contraction which may be confined to the trunk or to the face or 1 or more

extremities

6. Atonic Seizure Sudden loss of muscle tone lasting for seconds followed by post-ictal confusion Post-ictalperiod where the seizure stops Causes client to fall which may result in injury Aka Akinetic

2. Partial Seizure/Focal or Local Seizure- Neurologic abnormality may be limited to a specific part of the brain- Begins in 1 part of the cerebral hemisphere

1. Complex Partial Seizure Client loses consciousness or black out for 1-3 minutes and characterized by automatism (client is

not aware of the behavior) which may occur such as lip smacking, chewing, patting, picking at

clothes while in a dreamy state

After the seizure, the client may experience amnesia


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Psychomotor2. Simple Partial Seizure

Client remains conscious throughout the episode. He or she reports an aura before the seizuretakes place

During the seizure, client may have unilateral movement of the extremity, experience unusuasensation or have autonomic or psychic symptoms

Autonomic changes may include changes in heart rate, skin flushing, epigastric discomfort, pallor,piloerection (gooseflesh) pupillary dilation, tachypnea, sweating

3. Unclassified Seizure/Idiopathic Seizure- Accounts for about half of all seizure activity. They occur for no know reason and do not fit into the

generalized or partial classification

Causes of Seizure

1. Genetic- Defective genes for channels that regulate neuronal signal or the flow of ions in and out of the cell- Clients with progressive myoclonus are missing the cystatin B protein-

Familial tendencies***Cerebral Palsygenetic, may cause seizures

*** Febrile seizure caused by fever due to immaturity of hypothalamus

2. Acquired- Tetanus- Sepsis- Hypoxia/Anoxia- Prolonged Second Stage of labor (dystocia)- Cord coil- Hypothermia/Hyperthermia- Rabies, tetanus, meningitis- Metabolic disorders- Stress- Lack of sleep and stress- Children: birth injuries, anoxia, inflammatory brain lesions, CNS malformations- Adults: brain tumor, CVA/Heart Disease, metabolic disorders like uremia, hypoglycaemia,

hypocalcemia, excessive alcohol intake, emotional tension, fatigue, lack of food and sleep, intracrania

infection (encephalitis, meningitis, rabies, abscess, lead poisoning, monoxide poisoning)

3. Idiopathic- No known cause- Most often begins before the age of 20 years- 2/3 of cases

Phases of Seizure

1. Prodromal- Mood and behavioral changes

2. Aura- Earliest, serves as a warning


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3. Ictus/Ictal- Seizure actually occurs

4. Interictal- Interval between seizures

5. Postictal- Recovery phase- Seizures stops- Would rather go into sleep..accumulation lactic acid...depression of nervous system

Cerebral O2 utilization is about 3.5mL/min for each 100g of the brain. In the absence of O2, the cerebral function

can be supported for only 10 seconds before symptoms result

- 20% of O2 in the bodyGlucose consumption of the brain is 5.4mg /mL for each 100g of the brain. Brain can only survive 1-1 hours in the

absence of glucose before S/Sx of hypoglycaemia occurs

- 65-70% of glucose

Seizure Metabolism1. Production of ATP (only source of energy that can be utilized by the cell), the chief energy source of the

brain, increases by 250% to fuel the cellular sodium and potassium pumps, synthesize neurotransmitter

substances and transmit nerve impulses

In seizures, GABA dec, inhibiting control

2. Simultaneously, cerebral blood flow increases by 250% to facilitate CO2 removal and meet a 60% rise indemand for O2 (vasodilation)

3. Normal cerebral blood flow can meet such unusual metabolic demand for glucose and other nutrients aslong as hypoxemia, hypoglycaemia, or cardiac irregularities do not develop.

4. Seizures that include skeletal muscle contraction can bring on hypoxemia and hypoglycaemia throughincreased metabolic activity.

5. Under these conditions, available oxygen and glucose may be inadequate to supply the brain, then energydebts follow markedly diminished ATP and rising lactate levels causes cellular exhaustion and injury.

Pathophysiology

When the integrity of the neuronal cell membrane is altered cell membrane is altered

Cells begin firing wing increased frequency and amplitude and cant be controlled and modulated

Neuronal firing spreads to adjacent normal neurons particularly the brainstem and thalamus

Excitation of the cells/neurons causing sustained muscle contraction or depolarization and loss of consciousness

Eventually, inhibitory neurons in the cortex, anterior thalamus and basal ganglia slows the neuronal firing

Seizure is interrupted and produces an intermittent contraction an relaxation phase


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Once the epileptogenic neurons are exhausted (by lactic acid) and inhibitory neurons are exhausted and inhibitory

process build, the seizure stops (the client will be sleepy)

Depress CNS action and impairs consciousness

Diagnosis

1. EEG- most objective tool in the diagnosis- avoid stimulant e.g. coffee, not placed on NPO alter electrical activities of the brain

2. CT Scan3. MRI to rule out brain lesions4. PET Scan to measure cerebral blood5. Single-Proton Emission Computed Tomography to measure cerebral blood6. CSF Manometrics Lumbar tap7. Developmental Hx8. Skull X-ray9.

Blood studies

Medical Management

1. Muscle Relaxant- Diazepam (Valium) as long as there is no respi depressions

2. Anti-Epileptic Drugs/Anticonvulsant- Reduces responsiveness of the cerebral neurons to abnormal responses by blocking either some of the

neurotransmitters, some of the ion (Ca ions)

- Phenytoin (Dilantin) gingival hyperplasia- Valproic acid (Depakene) (increase the action of GABA)- Valproic Na (Depakote)- Clonazepam (Klonipine)- Phenobarbital (Luminal)- Carbamazepine (Tegretol)- Consider the blood levels of the drugs, check CBC reports, problems of drugs interaction use of

anticoagulants Vitamin K liver is compromised problem of prothrombin production

anticoagulants should be avoided; aspirin inhibits Phenytoin; antihistamine, sleeping pills inhibits

phenytoin

- Avoid alcohol- Oral hygiene- Take drug on time, avoid OTCs- Do not stop abruptly

***O2 if there is deficit

Antibiotics infection

Hypoglycemia juices, glucose injections, dextrose

Treatment of the underlying condition

Ketogenic diet high fats, low CHO ketones can be oxidized to produce energy


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Surgical Management

1. Cortical Resection/Corpus Callosotomy- Make seizures tolerable- Excision of 1 section of cortex to reduce the spread of epileptic dischargesComplication: Disconnection Syndrome pathways responsible for communication from 1 hemisphere to

another is severed can cause mutism

2. Temporal Lobectomy- Area in which seizures begin are remove without causing neurologic or cognitive deficitComplication: visual and language defects for a few weeks

3. Hemispherectomy- Removal of most of the cortex of 1 hemisphere in children with intractable seizures

4. Vagal Nerve Stimulator Implantation- Provides a stimulus that desynchronizes the abnormal uncontrolled electrical discharge of the brain

activity during a seizure

Hippocampus - memory

Nursing CareRisk for injury r/t uncontrolled movement

***Promote safety: raise padded side rails

***Avoid restraints in the client

***Avoid pillows that are not secured

***Padded tongue depressorinserted before the attack

***Turn head to the sides

***Remove braces or dentures

***Avoid driving or using heavy machinery

***NPO during attacks

***Diet as ordered

***Oral hygiene, gum massage

***Limit the visitors

Ineffective Airway Clearance

***Suction

***Wipe secretions

***Turn patient in side lying to prevent tongue collapse

***Semi-Fowlers

Impaired Gas Exchange/Impaired Tissue Perfusion

***Oxygenation

***HepLock for IV

Activity Intolerance/Impaired Physical Mobility

***provide adequate rest for patient


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***avoid strenuous activities

***energy saving environment, avoid stimulation

***assess clients mobility for appropriate mobility devices

Increase ICP seizures; sneezing, coughing, suctioning should be avoided

***Deep breathing and coughing exercises

Impaired Sleeping Pattern r/t outcome of disease process

Ineffective coping allow the client to verbalize, involve SO in planning; avoid labelling

Knowledge Deficit educate the client in taking medication, inform limitation in activity

Take note of time started and ended and turn to the side

Nursing Intervention1. Protect child from injury2. Observe and record seizure patterns3. Provide privacy during seizures4. Promote physical and mental health5. Reorient patient to his environment when he is fully conscious6. Patent airway during seizures

Multiple Sclerosis (Disseminated Sclerosis)

- Demyelination- Encephalomyelitis disseminata- Axon is involved- Schwann cell- Node of Ranvier- Affectation is on the myelin sheath found in the axon- Occurs in conducting pathways of brain and spinal cord- Chronic progressive demyelinating disease that affects the myelin sheath of the neurons in the CNS- Destruction of the myelin sheath- Degenerative disease affective twice as often as men- Occurs usually between 20-40 years of age- Impulses are slow and disrupted

Causes

1. Unknown2. Autoimmune

- T Lymphocytes (great role in autoimmune) can mistakenly see myelin sheath as a foreignmaterial, monocytes and some microglial cell (can act as macrophage)

3. Genetics Human Leukocytes Antigen A gene complex in chromosome 6


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4. Viral Infection Epstein-Barr Virus (most potent linked to MS)5. Environmental Factors

a. Emotional Stress dec IS, we are more prone to infectionb. Physical Injury or Trauma can be equated in problem in brain and spinal cord hypoxia can occu

in a specific area cerebral neuronal death/impairment brain cells does not regenerate

c. Infectiond. Pregnancy this causes stress

Clinical Manifestations

1. Initial Signs 3 common disorders related to brainstem involvement; pain- There is visual problems in patient with MS

a. Diplopiab. Optic Neuritis inflammation of the optic nerve

Blurred vision Color blindness Scotomas blind spots in the field of vision which can hamper visual perception of

clients Difficulty in seeing bright lights

c. Nystagmus2. Impaired Motor Function

- Due to cerebellar involvement- Fatigue is the most disabling and most common- Ataxia can occur uncoordinated body movement- Clumsiness- Weakness- Paralysis- Hyperreflexia increase reflexes-deep tendon reflexes- Paresthesia tingling sensation; pins and needles can be felt- Dysmetria inability to limit or direct movement- Dysdiadochokinesia inability to sop one motor impulse and substitute another

3. Nerve InvolvementA. Impaired Sensory Function

- Touch numbness- Pain (Hypalgesia diminished sensitivity to pain)- Temperature- Perception px may have Astereognosis

B. Bladder- Retention of incontinence (increase post residual volume)

C. Bowel- Constipation (problems in sphincter

D. Lhermittes Sign- Barber-chair phenomenon- Passive flexion of neck, there will be an electrical sensation or shock felt in the back of the head

radiating to the spine


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E. Trigeminal and Facial Nerve Involvement- Dysarthria slurred and scanning speech (disorder in articulation syllables are inappropriately

stressed)

- Dysphagia difficulty in swallowing check gag reflex- Altered Cough Reflex

F. Cranial Nerve and Brain Stem Involvement- Tinnitus- Hearing loss- Vertigo

4. Seizure- Flexor spasms at night, hyperactive deep tendon reflex- Client might go to the toilet to urinate

5. Psychosocial- Mood swings

6. Sexual Impotence in males and frigidity in females (altered sexual pattern)7. Advance cases: Dementia

-

Include short term memory loss, decreased ability to perform calculations, inattentiveness,impaired judgement

-Dysesthesia unpleasant/painful sensation upon stimulation of a sensory nerve

Eg Trigeminal Neuralgia Tic douloureux

Charcoats Triad

Scanning Speech (cerebellar and facial nerve involvement)

Intentional/Intention Tremor

Nystagmus

Multiple Sclerosis

Autoimmune response

Attack myelin sheath

Myelin sheath swells in response to toxic/metabolic changes

Breakdown of the myelin sheath releases free fats, local inflammation marked by accumulation lymphocytes

Glial cells proliferate and carry phagocytosis

Destruction of oligodendrocytes and Demyelination

Myelin sheath replaced with distinct fibrous plaque

Plaque impairs conduction along nerve fiber from one node of Ranvier to the next


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- Impaired motor function- Eyes disorders

- Nerve involvements- Seizures

- Memory loss- Sexual dysfunction

Medical Management

1. Treatment of Acute relapses in the acute stageA. Use ofCorticosteroids

- Such as methyprednisolone IV, oral prednisone- Anti-inflammatory, immunosuppressive

B. Immunosuppressants- Azathioprine (Imuran) Cyclophosphamide (Cytoxan)

2. Treatment aimed at disease management during exacerbationA. Interferon B1b (Betaseron)

-

Antiviral and immunoregulatory properties reducing the number of MS exacerbation- Injected subcutaneously every other day- S/E: ever, fatigue, and flu like manifestations

B. Interferon B1a (Avonex)- Reduce the number and severity of relapses- S/E fever, fatigue, and flu l ike manifestations

C. Glatiramer acetate (Copaxone)- Anti-inflammatory (synthetic)- S/E face flushing, DOB chest tightness- Does not manifest flu like symptoms

3. Symptomatic TreatmentA. Bladder Dysfunction- Oxybutin chloride (Ditropan)- Anti-spasmodic/anti-cholinergic- Propantheline bromide (Pro-Banthine)- Anti-spasmodic/anti-cholinergic

B. Constipation- Psyllium hydrophilic mucilloid (hydrocil, Metamucil), bisacodyl (Dulcolax)- laxatives

C. Fatigue- Amantadine (Symmetrel)

o Antiviral/antiparkinsonian agent/anticholinergic- Modafinil- CNS stimulant/relieves fatigue

D. Spasticity- Baclofen (lioresal)- Diazepam (Valium)- Dantrolene (Dantrium)


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o Muscle relaxantsE. Tremor

- Propanolol (Inderal)o Beta-adrenergic blockers

- Phenobarbital (luminal)o Anti-convulsant

- Clonazepam (Klonopin, Rivotril)o Anticonvulsant

F. Dysesthesias and Trigeminal Nerve Neuralgia- Carbamazepine (Tegretol)

o Anticonvulsant- Phenytoin (Dilantin)

o Anti-convulsant- Amytriptyline HCl (Elavil)

o TCAG. TENS (Transcutaneous Electrical nerve Stimulation)

-

Dysesthesias (numbness)- Areas of numbness are stimulated

***Evening primrose oilblood thinning propertyincrease circulation in certain area and sunflower oil

H. Rehabilitation- Physical, OT, Speech

Lab Test

- MRICT Scan

- Visual Evoke Responses- Visual Activity Test- Brain Stem Auditory Response- Electrophoresis- CSF Lumbar tap

Oligoclonal Bands are immunoglobulin sheet

Nursing Interventions

1. Provided bed rest fatigue r/t demyelination; rest during attack of MS (during exacerbation)2. Protect the client from injury by providing safety measures

- Hand rails- A well lighted room- Corrective glasses or eye patch in affected eye (Diplopia)- Avoid overly waxed floor- Avoid exposure to extreme temperature

o Check temperature of bath water3. Place an eye part on the eye for Diplopia4. Monitor potential complication such as UTI, calculuses, decubitus ulcers, RTI, and contractures


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*** ROM if the px is not tired

5. Promote regular elimination by bladder and bowel training best is twice a day6. Encourage independence7. Assist the client to establish a regular exercise and rest program8. Instruct the client to balance moderate activity with rest periods9. Assess the need for and provide assistive devices (walker, canes, wheel chair)10. Initiate physical and speech therapy11. Instruct the client to avoid fatigue, stress, infection, overheating and chilling12. Instruct the client to increase fluid intake and eat a balanced diet including low fat, high fiber foods and

foods high in potassium

Myasthenia Gravis

- A neuromuscular disease characterized by marked weakness and abnormal fatigue of voluntary musclesthat worsen with exercise and improves with rest

- Disturbance in the transmission of impulse from nerve to muscles at the myoneural junction- Problem lies in myoneural junction-

Motor end plate = nerve terminal- Depolarization contraction- Repolarization relaxation- Problem is in the transmission of impulses in the axon

Causes

Unknown Auto-immune

- Triggered b viral infection- Antibodies to the acetylcholine receptor sites causing decreased level of acetylcholine- Anti acetylcholine receptor site antibodies

Thymoma- Encapsulated thymus gland tumor 10-15%- Hyperplasia of thymus 70-80%- Thymus glands contained myoid cellsThymus gland

o H shaped bi-lobe organ in the root of the neck and in front of the hearto Contains myoid cells which has surface acetylcholine receptorso Infections or inflammatory conditions of the thymus gland may cause production of ant

acetylcholine receptor antibodies

Clinical Manifestations

A. Optic nerve, Oculomotor, Trochlear and Facial nerve involvement- Sleepy, apathetic weakness of the orbicularis ocular muscles- Bilateral ptosis (drooping of the eyelids) weakness of the levator palpebrae muscles- Double vision/Diplopia weakness of the extraocular muscles- Mask-like facial expression weakness of the levator palpebrae and facial muscles

B. Due to Glossopharyngeal, Facial, Hypoglossal nerve involvement


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- Dysarthria difficulty, weak voice, hoarseness- Attempt to smile turns to a snarl- May hold jaw to keep it close- Cough reflex impaired mucus and fluids cannot be expelled, palatal, pharyngeal muscles,

weakness (problem of aspiration)

- Difficulty in chewing and swallowingC. Due to the involvement of the diaphragm and intercostal muscles

- Respiratory difficulty decreased vital capacity and tidal volume can lead to respiratoryarrest/distress

D. Due to spinal accessory nerve/skeletal muscle involvement- Weakness of the neck and musclescant elevate and support head- Muscle weakness or fatigue in proximal limbs

Pathophysiology

Auto immune

Anti acetylcholine receptor antibodies

Attack the motor end plate/nerve terminal Acetylcholine receptor sites

Resulting to destruction of acetylcholine receptor sites

Less binding of acetylcholine reduced level of acetylcholine at receptor sites

Weakness of muscle contraction

S/Sx

Diagnostic Test

1. Tensilon test Tensilon short acting anticholinesterase drug 3-5 minute effectEdrophonium chloride

IV administration of Tensilon 2mg, if it is + MG, there is improvement of strength of px, administer

additional 8mg, a total of 10mg, px strength will be ok, lasts for 3 -5 minutes

2. Electrical Stimulation- Px will complain of fatigue if it is continued

3. X-ray of the Thymus gland can be done4. Cranial Nerve Testing

- Cranial nerves are affected in MS5. S/Sx manifested

Medical Management

1. Anticholinesterase drug/cholinergic increases levels of acetylcholine at the myoneural junction- Inhibits and inactivates acteylcholinesterase blocking the breakdown of acetylcholine at the

myoneural junction


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- Neostigmine bromide (Prostigmin)o Orally TID or QID

- Pyridostigmine bromide (mestinon)o IM 30-60mg effect last 204 hours

- Ambenonium Cl (Mytelase) 5mg every 4-6h- Be ready for anticholinergic drugs (may cause cholinergic crisis)- Taken with milk or food to prevent gastric distress

2. Corticosteroids directed toward reducing the levels of serum Ach receptor antibodies- Prednisone 60-80mg/day, 10-20mg/day- To reduce GI effects, antacids are given (consider as per doctors order)

3. Cytotoxic Drugs/Immunosuppressants- Chyclophosphamide (Cytoxan)- Azathioprine (Imuran)- Reduces circulating antiacetylcholine receptor antibodies

4. Plasmapheresis- Adjunct therapy-

Process where plasma is separated from formed elements of blood. Plasma is discarded, then PRBCis joined with Albumin, NSS, and electrolytes and returned to client

Purpose: To remove plasma proteins containing antibodies that are believed to cause MG

Potential Complications of Plasmapheresis are:

- Myasthenic or Cholinergic Crisis- Hypovolemia (Rarely)

5. Surgical ManagementThymectomy removal of thymus gland

- Indicated and recommended in the early phase of MG- Effect of Thymectomy is not fully understood, but it may alter immunologic control mechanism that

affect the production of antibodies to the Ach receptorMyasthenic Crisis

- SsMyasthenic Crisis Cholinergic Crisis

Insufficiency (Anti-cholinesterase drug under

dosage/Cholinergic drugs)

Decreased level of acetylcholine

Increase BP

Tachycardia

Restlessness

ApprehensionIncrease Bronchial secretion (suctioning/prone to aspi)

Sweating/Lacrimation

Generalized Muscle weakness

Absent cough reflex

Dyspnea (O2)

Difficulty in swallowing (NGT)

Difficulty in speaking

Bowel and bladder incontinence

Overdosage of Anticholinesterase

Increased level of Ach

Decreased BO

Bradycardia

-

--

-

-

Fasciculation

-

-

-

Abdominal Cramping


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Diarrhea

***Administer Tensilon emergency drug ***Atropine SO4, withhold acetylcholinesterase

Followed by Neostigmine bromide and Prostigmin (takes a longer)

Intervention

1. Encourage deep breathing and coughing exercises. Suction when necessary teach SO to suction2. Instruct client to sit upright when eating3. Provide ventilator support4. Plan activities carefully including rest periods.5. Provide client and family information about MG and treatment including adverse reactions of medication6. Explain how to recognize myasthenic and cholinergic crises and how to plan for medical help7. Avoidance of immobility problems for clients with severe MG especially if they become totally dependent

on Nursing care for ADL; avoid strenuous activities

Fatigue

Activity

Ineffective airway clearance

Exercise after giving cholinesterase

Knowledge deficit plan health teaching, tx and medications that should be avoided muscle relaxants,

sedatives, narcotics, aminoglycoside (streptomycin, gentamicin) block neuromuscular transmission

8. Neuro assessment LOC, CephalocaudalParkinsons disease

- Paralysis Agitans- Client has with problems with rigidity not true paralysis- Non intentional tremors- Boxers Disease-

Dr. James Parkinson noticed tremors that can be manifested by the px- A chronic progressive neurologic disorder that results from the loss of neurotransmitter Dopamine in a

group of brain structures that control movement

- Inhibitory Dopamine produced in the substantia nigra in the basal ganglia- Results from the degeneration of nerve cells in the basal ganglia particularly the substantia nigra and corpus

striatum resulting in generalized decline in muscle function

- An extra pyramidal system disorder essential component of total movement (Relaxation, stabilizationadjustment and posture)

- Pyramidal primary movements- Basal ganglia helps control body movements and rely on dopamine- Dopamine is produced in the substantia nigra, adrenal gland, kidney and has an inhibiting function in the

central control movement; dopamine cannot pass blood brain barrier Excitatory to CVS

- Nigrostriatal tract neural tract that connects the striatum and the substantia nigra- Corpus striatum stores the dopamine there should be equal amount of Ach in the corpus striatum- In normal brain, the levels of dopamine and acetylcholine are evenly balanced- Chemical imbalance: In Parkinsons disease the levels of dopamine reduce and ACH over reactive as

manifested as tremors

- 60-70 years of age


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Causes

a. Unknown genetic extra copy of a normal gene (SNCA) Alpha sinuclein causes too much build up ofprotein in the brain

- Gene Parkin responsible for the degradation of some of the neuronal proteins releasing freeradicals; build up of protein in the brain

b. Toxic carbon monoxide poisoning, lead, manganese, mercury- Endotoxin (Lipopolysaccharide) LPS airborne environmental contaminant in agriculture and rice

industries

- Well water consumption (those living near wood mills) because of chemicals used in the dryingproducts

c. Atherosclerosis, Arteriosclerosis- Diminished blood supply to the brain affecting basal ganglia leading to degeneration of nerve cells

d. Traumatic- Midbrain compression- Basal ganglia is a midbrain nucleus

e. Drug induced Reserpine-

Rauwolfia Alkaloids deplete dopamine- Phenothiazines block dopamine receptors

o Haloperidol, Chlorpromazine, Thioridazinef. Oral Contraceptives contain estrogen hormone causing increased blood viscosity thrombus formation

less blood supply

g. Viral infection may attack the basal gangliah. DiabetesMellitus peripheral circulation impaired decrease glucose to the brain affecting the basal ganglia

Clinical Manifestation

Six Cardinal Signs:

1. Tremors at rest common early sign2. Rigidity general feeling of stiffness3. Bradykinesia/Akinesia4. Flexed posture of the neck, trunk and limbs shuffling, propulsive gait5. Loss of postural reflexes6. Freezing movement

Key Features of Parkinsons Disease

Posture

- Stooped posture- Flexed trunk- Fingers abducted and flexed at the metacarpophalangeal joint - Wrist slightly dorsiflexed

Gait

- Slow and shuffling- Short and hesitant steps- Propulsive gait (stop and retropulsive gait)- Festinating smaller quicker steps- Difficulty stopping quickly


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Motor

- Bradykinesia- Akinesia- Tremors- Pill rolling movement of index finger and the thumb- Mask like faciesParkinsons mask (eyes wide open and seems to stare) - Difficulty chewing and swallowing- Uncontrollable drooling of saliva, esp at night- Fatigue- Difficulty in and out of bed - Little arm swinging when walking- Chang in hand writing (Micrographia)- Rigidity

Speech

- Soft low pitch voice (microphonia)- Dysarthria slurred speech-

Echolalia automatic repetition of what another person says; Repetition of sentences- No change in voice volume, phonation or articulation monotonous voice

Autonomic Dysfunction

- Orthostatic hypotension- Excessive perspiration- Oily skin- Seborrhea- Flushing- Changes in textures- Blepharospasm (eyelid spasm)

Psychosocial- Emotional lability- Rapid mood swing- Paranoia- Easily upset- Rapid mood swing- Cognitive impairments (dementia)- Delayed reaction time- Sleep disturbances


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Pathophysiology

Degenerative Disorder/Other Factors

Degeneration of Basal Ganglia in Midbrain

Loss of Neurons (Dopamine)

Dec Dopaminergic Neurons

Depletion of Dopamine

Alteration in Muscular Function (6 Cardinal Manifestation)

Diagnostic Test

- No specific test for Parkinsons Disease- ECG and CT Scan to r/o other neurologic disorders- U/A Dopamine level can be detected- 65-400mg/24 hours

Medical Management

- Non Curative1. Anti-Parkinsonian Agents (Dopaminergic)

-

Improves muscle flexibilitya. Levodopa

o Increased levels of dopamine in the braino Relieves tremors, rigidity and Bradykinesia

- S/E:o Anorexiao N and Vo Postural Hypotensiono Mental changes such as confusion, agitation and hallucination

o Avoid multivitamin preparation containing B6, Pyridoxine, and foods high in Vit. B6 blocksdesired action of Levodopa (tuna, pork, dried beans, salmon, beef, and liver.

o Administer with food or snack to avoid GI irritationo Inform the client that the urine and sweat will be darkened

b. Sinemeto Carbidopa with Levodopao Carbidopa reduces destruction of Levodopa at the periphery. Inhibits enzyme

Dopadecarboxylase thereby preventing breakdown of dopamine at the periphery allowing

the L-Dopa to reach the brain

o Causes fewer S/E like dyskinesia, paranoia, aggressive behavior2. Dopamine Agonists/Antiviral

- Dopamine receptor agonistsa. Amantadine HCl (Symmetrel)

o Blocks the reuptake of dopamine at the synaptic cleftb. Bromocriptine (Parlodel) crosses the blood brain barrier stimulate the release of dopamine in

the substantia nigra. Often employed when the L-Dopa loses effectiveness

c. Pergolide (Permax)d. Pramipexole (Mirapex)e. Ropinirole (Requip)


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3. COMT Inhibitors COMT inhibitors inhibit Cathecol-O-Methytransferase (COMT) which is responsible formetabolizing dopamine. Administration of a COMT inhibitor with Levodopa increase the amount of Levodopa

available to the brain to control Parkinsons

Tolcapone (TASMAR)

Entacapone (CONTESS)

4. Monoamine Oxidase (MAO) Inhibitors- Selegiline (Eldepryl, Deprenyl)- Selegiline works by selectively inhibiting the enzyme that inactivates dopamine in the brain- Check for orthostatic Hypotension, changes in movement, hallucinations and confusion- Assess for hypertension which can occur with higher than usual doses- Enhances norepinephrine activity- Avoid tyramine-rich food foods

5. Anticholinergics- Block the excitatory action of neurotransmitter acetylcholine- Ease drooling, tremors and rigidity- Benztropine mesylate (Cogentin)-

Biperidin (Akineton)- Trihexyphenidyl HCl (Artane)- S/E are blurred vision, dry mouth, constipation, delayed gastric emptying, urinary retention, photophobia

and tachycardia, confusion, depressions, delusion and hallucinations

- Should be tapered slowly when discontinued6. Antihistamine

- Diphenhydramine (Benadryl) to decrease tremors and anxiety7. Antidepressants to improve mode since serotonin levels is decreased

- Chlordiazepoxide (Librium)8. Physical Rehabilitation

- May develop contracture9. Surgerya. Pallidotomy destruction of the globus pallidus using electrical stimulation (use of cautery, injection of

alcohol, or by cryogenic surgery by cooling or freezing by use of liquid N)

- Done to relieve rigidityb. Thalamotomyc. Deep Brain Stimulation placement of electrodes in the thalamus then attaching to a pulse generator

implanted in the intraclavicular region to relieve tremors

d. ExperimentalAdrenal tissue transplant implantation of adrenal medullary tissue into the corpus striatum to re-

establish normal dopamine release by dopamine producing cells into the caudate nucleus

Stem cell transplant provide viable dopamine producing cells into the caudate nucleus

- From cord blood


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Nursing Diagnoses and Nursing Management

1. Risk for injury: Provide a safe environment r/t blurred vision, Bradykinesia, incoordination- Side rails up on bed- Hard back chair for support- Wear good, sturdy shoes- Use cane or walker- Concentrate on standing upright- Make sure you have an adequate lighting- Remove all throw pillows, rugs, electrical cords and clutter- Assist client in ambulation- Avoid sharp objects- Avoid overly waxed floors

2. Impaired physical mobility: Provide measures to increase mobility r/t Bradykinesia, rigidity, freezing movement,cogwheel rigidity

- Physiotherapy (PROM and AROM)-

Provide assistive devices- If client freezes mental thoughts- Assistance of activities with daily living- Rock back and forth to get going- Imagine you are stepping over an imaginary line when walking- Count to yourself while walking- Visualize tour intended movement

3. Altered Self Concept: Encourage independence or powerlessness r/t inability to perform ADL- Alter clothing for ease in dressing (use zipper or Velcro) avoid laces, buttons- Do not rush client- Perform self-care activities- Give emotional support- Give client time to finish activities

4. Impaired Verbal Communication: provide measure to improve speech r/t microphonia- Encourage to practice reading aloud, listen to own voice- Refer to speech specialist- Pause between every few words- Exaggerate the pronunciation of words- Finish saying the final consonant of the words before starting to say the next word- Express ideas in short, concise phrases- Plan what to say- Face the listeners- To keep saliva from building out into your mouth: make a conscious effort to swallow saliva- Keep your head in an upright position so saliva will collect in the back of the throat and stimulate automatic

swallowing

- Swallow excess saliva before attempting to speak5. Alteration in nutrition less than body requirements: provide a well-balanced diet r/t dysphagia

- Cut food in small, bite size pieces


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- Provide small, frequent feedings- Allow sufficient time for meals- Increase caloric needs- Adding commercial powders to thicken liquid- Upright positioning- Weigh client- Serial monitoring of Se albumin and protein levels to check for malnutrition Se Albumin 3.5-5g/dL or 35

50g/L

Se Protein 68-83g/L

- Keep lips closed- Put food in your tongue- Lift your tongue- Eat slowly, taking small bites- Finish your bite before taking another

6. Altered Bowel Elimination r/t constipation, immobility- Encourage mobility-

Increase fluid intake- AdministerLaxative (check for bowel sounds, how many days, refer client to the doctor)- Increase fiver in the diet

7. Knowledge Deficit about the disease process provide information about the disease- Nature of the disease- Prescribed medicines ad side effects- Importance of daily exercises- Limit postural deficiencies (firm mattress)- Promotes active participation in self care- Lie down on hand with tremors- Tremors: hold change in your pocket or squeeze a small rubber ball

o Used both hands to accomplish tasko Lie down on the floor. Relax entire bodyo Sleep on side that has the tremor

- Trouble getting dressed: dress and undress in from of the mirror. Buy clothes with self fastener like Velcroor slide-locking buckles

Cerebrovascular Accident

WHO Definition: Stroke

- A neurological deficit of sudden onset accompanied by focal dysfunction and symptoms lasting more than24 hours that are presumed to be of a non-traumatic vascular origin

WHO Definition: Transient Ischemic Attack

- Neurological events that have a duration shorter than 24 hours, followed by complete return to baselineFacts

- Leading cause of adult disability- 3rd leadin cause of death in the Use- 75% of all strokes occur in patients >65 years of age


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Risk Factors

- Hypertension primary cause- Atrial fibrillation- Increasing age (particularly >65)- Cigarette smoking - vasoconstriction- Unmanageable diabetes- High cholesterol >240g/dL- Obesity- Hx of TIA- Male gender

Pathophysiology

- Cerebral blood flow provides brain with O2 and glucose for energy at rate of 40-60mL/100g of brain/min- When rate is subarachnoid hemorrhageo Occur during stress or excretiono Focal deficits rapidly evolveso Confusion, coma or immediate deatho One month mortality


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o 50% for SAHo 80% for intracerebral hemorrhageo More often intracerebralo May occur as a result of aneurysmPremonitory S/Sx

1. Nape pain2. Severe headache3. Blurred vision4. Altered LOC (Confused, light headedness, fleeting loss of consciousness5. Slurred speech6. Inc BP7. Transient local sensory deficit (loss of sensation, paresthesia)8. Weakness (Paresis)

Assessment

1. Motor loss (paresis - hemiparesis, plegia - hemiplegia)2. Sensory loss/deficit

***anosmia absence of sense of smell***Agnosia inability to recognize familiar objects through

***Astereognosis inability to recognize

***Hypalgesia

***urinary retention or incontinence

***constipation or incontinence

***alalia inability to speak because of damage in the vocal cords

***alexia inability to read

***dyslexia problem in reading

3. Impaired verbal communications***slurred speech Dysarthria (difficulty in speaking)

***aphasia a disturbance in the communication ability to read, write and interpret messages

Receptive Wernickes aphasia (Fluent can speak but cannot understand or interpret

messages)

Expressive Brocas aphasia (Non fluent Difficulty in articulation; can understand but

cannot speak)

Globalboth

4. Impairment of the mental ability and psychological effects (behavioral changes)- Left hemisphere affectation slow cautious and disorganized

- Right non-dominant impulsive, overestimate ability an decreased attention span

- Right patterns of perception and artistic form of intelligence

- Left analytical and verbal skills

5. Visual DeficitsHomonymous hemianopia/psia blindness in the of the visual field

Left homonymous problem in the right optic tract


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***Horners Syndrome ptosis of the eyes; sinking of the eyeballs; blinking reflex is affected; may

cause drying of the cornea; constriction of the pupils and the lack of tearing in the eye

Pathophysiology

Aneurysm

Increased Pressure in the BV

Increased Thinning of the walls of the BV/Artery

Ruptures of the BV

Bleeding/Hemorrhage

Loss of blood supply to the brain

Hypoxia

Cerebral Ischemia

Irreversible brain damage or infarction

Alteration in cerebral metabolism

Cell death and permanent changes

S/Sx Motor loss, sensory deficit, visual impairment, impaired verbal communication, behavioral changes

***Decussation 90% in medulla oblongata

Laboratory Test

Neurologic Exam

GCS, Deep Tendon Reflexes

Imaging Exam

MRI

CT Scan

Cerebral AngiographyCBC Hgb/Hct

PT

PTT

Lumbar Tap as long as no impending increase in ICP; to check for blood in the CSF

EEG/EKG

Se Electrolytes

Glucose level of the Client FBS depending on the case

Medical Management

1. ThrombolyticsrtPA Recombinant Tissue Plasminogen Activator

- can be given through IV- not given to client with intracerebral hemorrhage

Enoxaparin (Clexane)

2. Anticoagulant- In cases of cerebral thrombosisHeparin, Aspirin, Warfarin


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3. Osmotic DiureticK Sparer/K Waster

- Monitor client carefully- Mannitol

4. Vasodilators- Nimodipine- Amlodipine- Nifedipines

5. Antihypertensives- Beta-blockers- Hydralazine (Apresoline)

6. Anxiolytics- Can be given as long as the GCS is ok - C/I in coma- No respi depress

7. H2 Blocker-

Ranitidine (Zantac)- Cimetidine (Tagamet)- Famotidine (H2-Bloc)

8. Laxatives9. Antifibrinolytic Agent

- Epsilon Aminocaproic Acid (Amicar) EACA10.Antibiotics11.O2 administration12.IVF on unaffected side13.NGT14.Catheterization15.Surgery

Carotid Endarterectomy

- Surgical excision removes atherosclerotic plaques from the inner arterial wall, most commonly theinner arterial wall, most commonly at carotid arterial bifurcations

Extracranial/Intracranial Bypass

- Splicing an extracranial artery (such as the superficial temporal artery) to an intracranial artery(such as the MCA) bypasses an occlusion

16.Rehabilitation- As soon as the client enters the hospital

Nursing Management

Elevate the head of the bed r/t

Impaired Tissue perfusion r/t decrease blood flow to the brain

Impaired gas exchange

Ineffective airway clearance r/t secretions

Impaired physical mobility r/r right sided weakness

Impaired sensory perception


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Fluid volume excess/deficit

Impaired verbal communication r/t involvement of the facial and trigeminal nerve

Powerlessness

Disturbed body image

Activity Intolerance

1. Ineffective tissue perfusion: cerebral- Monitor N V/S- Maintain BP- Elevation of bed to 30 degrees

2. Risk for aspiration- Assess for S/Sx of aspiration- Feed cautiously- Monitor CXR results- Allow time for feeding

3. Impaired Physical Mobility-

Encourage bed exercises- Promote walking, teach bracing- ROM

4. Risk for Impaired Skin Integrity- Skin assessment q2h- Change position q2h

5. Risk for contractures- Assess ROM in joints- Log rolling technique

6. Self-care deficit- Encourage to perform self care activities- Eye patch (alternate) if with Diplopia

7. Risk for Injury- Side rails up- Frequent skin infection- Assistance with ADL

8. Imbalanced Nutrition: Less than body requirements- Assess diet, ensure nutrition- Observe choking precautions- Proper positioning- Promote head control- Help/assist with swallowing

Interventions during acute-phase of CVA

1. Maintain patent airway and administer oxygen as prescribed2. Monitor V/S3. Maintain BP of 150/100mmHg to maintain cerebral perfusion


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4. Suction Fluids as prescribed, but never suction nasally and for longer than 10 seconds to prevent increasedICP

5. Monitor from increasing ICP because the client is most risk during the first 72 hours following CVA6. Position the client on the side, with head of bed elevated 15-30 degrees as prescribed7. Monitor LOC, pupillary response, motor and sensory response, cranial nerve function and reflexes.8. Maintain a quiet environment, and provide minimal handling of client to prevent further bleeding9. Insert a foley catheter as prescribed10.Administer intravenous fluids as prescribed11.Maintain fluid and electrolyte balance12.Prepare to administer anticoagulants, antiplatelet, diuretics, antihypertensives, and anticonvulsants

Interventions in the post acute phase of CVA

1. Continue interventions from acute phase.2. Position client 2 hours on the unaffected side, 20 minutes on teh affected side.3. Position the client on prone position if prescribed, for 30 minutes 3 times daily.4. Provides skin, mouth and eye care.5.

Perform passive range of motion exercises.

6. Place anti-embolism stockings on the client.7. Measure thigh and calves for an increase in size and assess for positive Homans sign 8. Monitor gag reflex and ability to swallow9. Provide sips of fluids and slowly advanced diet to foods that are easy to chew and swallow10.Provides soft and semisoft and fluids rather liquids because CVA client is better able to tolerate these types

of food

11.When the client is eating, position the client sitting i n a chair or sitting up in bed with the head and neckpositioned slightly forward and flexed

12.Place food in the back of the mouth on the unaffected side to prevent trapping of food in the affectedcheek

Intervention in the Chronic Phase of CVA

1. Neglect syndromea. Client is unaware of the existence of his or her paralyzed side (unilateral neglect)b. Teach the client to touch and use both sides of the body

2. Hemianopsiaa. Client has blindness in the same visual fieldsb. Homonymous Hemianopsia is blindness in the same visual field of both eyesc. Encourage client to turn the head to scan the complete range of vision; otherwise, he or sheer does

not see half of the visual field

3. Approach the clients on unaffected4. Place clients personal objects within the visual fields5. Provide eye care for visual deficits6. Place a patch over the affected eye if the client has Diplopia7. Increase mobility as tolerated8. Encourage fluid intake and a high fiber diet9. Administer stool softeners as prescribed10.Encourage client to express feelings


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11.Encourage independence in activities of daily living12.Assess the need for assistive devices such as cane, walker, splints, or braces13.Teach transfer technique from bed to chair and to bed14.Provide gait training15. Initiate physical and occupational therapy16.Refer client to a speech and language pathologist

Hemiplegia

Frozen shoulder

Subluxation of the shoulder

Painful shoulder hand dystrophy

Adduction of arm with internal rotation

Flexion of elbow wrist and fingers

External rotation of leg at hip joint

Flexion at knee; and

Plantar flexion and Supination at ankle

Shortened heel cord

Head Injury

- Any trauma to the skull resulting in varying degrees of injury to the brain by compression, tension orshearing force

- An insult to the brain that is capable of producing physical, intellectual, emotional, social and vocationachanges

Causes

- Motor vehicle accidents leading cause- Assaults- Falls- Sports related injuries

Risk Factors

- Alcohol- Driving without seat belt

Mechanisms That Contribute to Head Injury

- Penetrating injury that may fracture the skull- Diffuse injuries which do not result in fractures- Rebound of cranial contents that may result in an area of injury opposite the point of impact (Counter

Coup Injury)

Classifications of Brain Injuries:

- Open Injury a break in the scalp, skull, dura which exposes the brain to environmental contaminant- Closed Injury no break in the protective chamber: Contusion

Specific Types of Injuries (Primary Injuries)

1. Concussion- Violent jarring of the brain within the skull


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- Can cause temporary loss of consciousness2. Contusion

- Bruising injury of the braino Coup slower moving contents of the cranium strikes bony prominences of durao Counter-Coup moving head strikes fixed object and brain rebounds striking opposite side

of cranium

3. Laceration/Abrasion- Traumatic tearing of the cerebral cortex

4. HemorrhageEpidural Hematoma

- Forms between skull and Dura matter- Most serious hematoma because there are a lot of BV- Occurs rapidly

Manifestations

- Client usually unconscious immediately after head trauma - Client awakens and is quite lucid-

Changes in LOC occurs and pupil dilation response rapidly deteriorates- Client lapses into a coma- Client may have signs of vomiting- Severe headache- hemiparesis

***ipsilateral pupil dilation same side of the injury pupil dilation occurs

Subdural Hematoma

- Collection of blood in the subdural space (between the Dura and arachnoid matter) Classification

Acute

SubacuteChronic

Category Time Frame Density on CT

Acute 1-3days Hyperdensity

Subacute 4days to 3weeks Isodense

Chronic 3weeks 4months Hypodense

Manifestations of Acute Subdural Hematoma

- LOC after head injury- Headache for conscious clients- Irritability and confusion- Fluctuating LOC or may lapse into a coma- Development of lateralizing changes (client may have neurologic deficits)- Manifestation of neurologic deterioration- Headaches- Changes in LOC- Ipsilateral pupil dilation or fixation may deteriorate to fixed dilated

Intracerebral Hematoma

- Occurs less often than epidural or subdural hematoma


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- Hemiplegia more common than hemiparesis- Delayed Traumatic Intracerebral Hematoma hematoma that occurs after a few days

5. FractureTypes of Skull Fracture

1. Linear Skull Fractureo Single clean break

2. Depressed Skull Fractureo Pushes bony fragments toward the brain

3. Comminuted Skull Fractureo Splinters or crashes skull into many bone fragments

4. Basal Skull Fracture/Basilar skull fractureso Occurs at the base of the skull; usually the anterior and middle fossae which involves the

petrous portion of the temporal bone; more serious than fractures located elsewhere in

the cranial vault

S/Sx

o Cerebrospinal rhinorrhea and otorrhea associated with dural laceration should containglucose

Halo Sign blood in the center and outside is clearo Periorbital ecchymosis (Raccoons eyes)o Mastoidal ecchymosis (Battles sign)

5. Ethmoid Bone fractureClinical Manifestation

1. Skull fractureso CSF or other fluid draining from ear or noseo Blood behind tympanic membraneo Periorbital ecchymosiso Bruise over mastoid processo Indication of cranial nerve and inner ear damageo Facial paresiso Vertigoo Nystagmus

2. Concussiono LOC for 5 min or less, transiento Retrograde amnesia can remember the past but not the presento Post traumatic amnesiao Headache, dizzinesso N/Vo Irritability, lethargy

3. Contusiono Cerebral contusion: Hemiparesiso Brain Stem Contusion

Unresponsiveness Coma Cranial nerve dysfunction


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o Speech disturbance such as temporary aphasiaAssessment

1. Level of Consciousness- Be careful that alcohol ingestion, certain drugs and other pathological conditions complicate

patients LOC

- Increased ICP Glasgow Coma Scale; the shorter the loss of consciousness the better the prognosis2. Respiratory Pattern

- It is essential for the nurse to evaluate and record all qualitative characteristics of respiration notjust quantity

- Cheyne Stokes Respiration upper brain stem damage- Irregular respiration medulla- Slow labored breathing increase ICP

3. Pupils size and reaction- N is 2-3mm- N is consensual pupil dilatation- Ipsilateral dilated pupil (unilateral dilation and same side as brain injury)-

3

rd

cranial nerve compression (Oculomotor)- Midposition flexed pupil (Midbrain)- Pinpoint fixed pupil (pontine damage)

4. Eye movement and Oculovestibular Response- Nurse should note the position of eyelids and spontaneous eye movement- Observe if blinking is present

5. Motor Response from Skeletal MuscleA. Decorticate Rigidity

o Cortex of the brain is affectedB. Decerebrate

o Postural attitude characterized by upper brain stem damage6. Assess for Rhinorrhea, Otorrhea and Nuchal rigidityRhinorrhea fracture of Ethmoid bone

Otorrhea fracture of the temporal bone

- Glucose is present in CSF but not in mucus- ***Check discharges halo sign: - bloody spot surrounded by pale ring- Battles sign doesnt appear until 24-48 hours after injury, discoloration in the mastoid area

behind the ear

- Raccoon Eyes7. Assess for headache, nauseas and vomiting, Diplopia

- Monitor V/S reflecting increased ICP or shock (Increased temperature, increased BP, widenedpressure, decreased PR, decreased RR)

- Cushing sign (inc BP, dec PR and RR)- Inc BP accompanied by tachycardia is common in px with severe head injury (compensatory

responses of the body to supply blood to the brain against pressure in rising ICP)

- Diplopia (pressure at CNVI Abducens which controls the lateral rectus muscles)- 4-15mmHg N ICP pressure

8. Identify any overt or skull trauma


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Pathophysiology

Penetrating trauma (knife, sharp, objects)

Laceration associated to hemorrhage and edema

Destroy brain tissue

Limited regenerative capacity of CNS

Irreversible neuronal death

Extensive damage (gunshot wound)

Shockwaves that precedes bullet path through the brain

Tissue damage, compression of brain against skull

Contusion

Communicating Hydrocephalus

Non-communicating Hydrocephalus extraventricular

Diagnostic TestX-ray

CT Scan

MRI

CBC because of blood loss

Medical Management

- Airway- Breathing- Circulation- Immobilization (Cervical collar)- Protection from possible complications antibiotics; corticosteroids; osmotic diuretics; laxative;

vasodilators; anticonvulsants; analgesic;

- Oxygenation and lowering ICP- Fluid therapy/IV line- Observe for other injuries- For every F 6% decrease in ICP

Medications

1. Antibiotics2. Corticosteroids prednisone3.

Osmotic diuretics4. Laxatives

5. Vasodilators6. Antihypertensives7. Anti-tetanus prophylaxis HTIG; ATS8. Anticonvulsants

Nursing Management

- Assess and document V/S and neurologic status


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- Careful history taking from witness- Prompt recognition and treatment of hypoxia- Control increase ICP (Mannitol) avoid strenuous activities, bending, avoid valsalva maneuver- Stabilization of other conditions

Surgical Management

- Observe for risk of extradural hemorrhage- Craniotomy and elevation of depresses skull fractures- Craniectomy (if comminuted)/Cranioplasty- Shunting

Rehabilitation

- Physical therapy- Occupational therapy- Speech therapy- Cognitive therapy

curative and rehabilitative ncm of client with neurologic disorders

Documents