Neuro Nursing Ms.

Jean Javier

Curative and Rehabilitative NCM of Client with Neurologic Disorders Overview of the anatomy and physiology of the nervous system 1. Supporting Structures a. Skull b. Meninges c. CSF d. Blood Brain Barrier e. Blood Supply 2. CNS a. Brain b. Spinal Cord 3. PNS a. Cranial nerves b. Spinal nerves o Somatic o Autonomic Sympathetic Parasympathetic Neurologic Disorders 1. 2. 3. 4. 5. 6. 7. 8. 9. Seizure Disorders MS MG (Acetylcholine is affected in this disease) Parkinsons disease (Paralysis agitans) CVA stroke or brain attack; altered blood supply to the brain Alzheimers Disease lack of neurotransmitters and the role of toxic Al Headache attention headache or muscular headache or migraine headache Head Injury Spinal Cord Injury (SCI)

Outline Per Disorder o o o o o o o o Definition Nursing assessment S/Sx Lab dx Med mgt N mgt NCP Case analysis

Diagnostic Studies 1. Skull and Spinal radiography

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Neuro Nursing Ms. Jean Javier

2. 3. 4. 5. 6. 7. 8.

Computed tomography scan MRI Lumbar Puncture Myelogram Cerebral Angiography EEG 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 upper centers 2. Specialized tissues less able to survive when there is problem or deficit such as less oxygenation; brain cells does not regenerate 3. When there is a destruction those remaining are unable to replace those that are lost Eg. 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 part can 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 Structures 1. 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 bones Maxillae - 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 - Fontanels i. Anterior fontanel 9-18 months ii. Posterior fontanel 2-3monts - Head circumference is usually 1.25-2.5cm larger than the chest circumference; if the head size 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 Cloak like Venous sinuses b. Arachnoid Mater Thin and delicate Lies between the dura and pia Avascular composed 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 brain

Gyrus/gyri elevated, coil Sulcus/sulcus shallow/depression 3 Potential Spaces Within the Structures of Meninges 1. Epidural Space - bundle of nerves ; lots of BV crossing the epidural space; epidural hematoma can occur fast if there is an injury - external to dura 2. Subdural Space between Dura and arachnoid; hematoma can occur 3. Subarachnoid Space between arachnoid and pia; potential space where CSF circulates under N conditions 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 ml is 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 ventricles RLV LLV Right cerebral hemisphere Left Cerebral hemisphere There is a foramen in between known as Foramen of Monro; aka Interventricular Foramina going to 3rd Ventricle (slit like space between the thalamus) produces its own CSF Aqueduct of Sylvius going to th 4 Ventricle (located between the pons and the cerebellum) 3 openings in the roof of the 4th 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 sides and 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, essential 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 an injury/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, allows this 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 arteries The 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

Neuro Nursing Ms. Jean Javier

Central Nervous System (Brain-Spinal Cord) Brain Protection: Skill Nerves: Cranial 12 Motor: 5 Sense: 3 Moto/Sense: 4

Spinal Cord Location Cervical Thoracic Lumbar Saccral Coccyx No. of Pairs 8 12 5 5 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 and affection - Concentration, abstract thought, information storage and memory Brocas Area left side motor speech (word formation) resulting to slurred speech Expressive 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 and Brocas are affected Global Aphasia may result d/t CVA or any injury 4. Occipital Lobe visual area b. 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 o Maintains homeostasis Unconscious control Innervate involuntary functions of the body Sympathetic - Origin: Thoracic/Lumbar - Response: Involuntary - Fight or Flight Response - Sympathetic = Thoracolumbar T1-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 Parasympathetic - Origin: Brain/Sacral - PC Craniosacral Division - Cholinergic ~ Anabolic - D Division Digestion, Diuresis, Defecation - Response: Normal - Decrease everything except GIT, GUT - Vasodilation, Bronchoconstriction - Acetylcholine

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

Neuro Nursing Ms. Jean Javier

Spinal Nerves Cervical Thoracic Lumbar Saccral Coccygeal

1-8 1-12 1-5 1-5 1 31

C1-C7-exit above corresponding vertebra ***C8-below C7 and above T1 T1-Coccygeal below 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 wave Convulsion 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, convulsive movements and behavioral abnormalities - Chronic recurrent disorders - Recurrent seizures - A single seizure cannot contribute to an epileptic attack take note of the clients history Status Epilepticus - Consist of a train of severe seizure with relatively short intervals or not intervals between one seizure to another - 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 surface 1. 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 Cry is 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 patient 2. 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-ictal period 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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Psychomotor 2. Simple Partial Seizure Client remains conscious throughout the episode. He or she reports an aura before the seizure takes place During the seizure, client may have unilateral movement of the extremity, experience unusual sensation 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 Palsy genetic, 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, intracranial 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 body Glucose 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 Metabolism 1. 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 in demand for O2 (vasodilation) 3. Normal cerebral blood flow can meet such unusual metabolic demand for glucose and other nutrients as long as hypoxemia, hypoglycaemia, or cardiac irregularities do not develop. 4. Seizures that include skeletal muscle contraction can bring on hypoxemia and hypoglycaemia through increased metabolic activity. 5. Under these conditions, available oxygen and glucose may be inadequate to supply the brain, then energy debts 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 Scan 3. MRI to rule out brain lesions 4. PET Scan to measure cerebral blood 5. Single-Proton Emission Computed Tomography to measure cerebral blood 6. CSF Manometrics Lumbar tap 7. Developmental Hx 8. Skull X-ray 9. 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 discharges Complication: 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 deficit Complication: 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 Care Risk 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 depressor inserted 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 Intervention 1. Protect child from injury 2. Observe and record seizure patterns 3. Provide privacy during seizures 4. Promote physical and mental health 5. Reorient patient to his environment when he is fully conscious 6. 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. Unknown 2. Autoimmune - T Lymphocytes (great role in autoimmune) can mistakenly see myelin sheath as a foreign material, 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 infection b. Physical Injury or Trauma can be equated in problem in brain and spinal cord hypoxia can occur in a specific area cerebral neuronal death/impairment brain cells does not regenerate c. Infection d. 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. Diplopia b. 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. Nystagmus 2. 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 Involvement A. 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 stage A. Use of Corticosteroids - Such as methyprednisolone IV, oral prednisone - Anti-inflammatory, immunosuppressive B. Immunosuppressants - Azathioprine (Imuran) Cyclophosphamide (Cytoxan) 2. Treatment aimed at disease management during exacerbation A. 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 like manifestations C. Glatiramer acetate (Copaxone) - Anti-inflammatory (synthetic) - S/E face flushing, DOB chest tightness - Does not manifest flu like symptoms 3. Symptomatic Treatment A. 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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Muscle relaxants

E. 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 TCA G. TENS (Transcutaneous Electrical nerve Stimulation) - Dysesthesias (numbness) - Areas of numbness are stimulated ***Evening primrose oil blood thinning property increase circulation in certain area and sunflower oil H. Rehabilitation - Physical, OT, Speech Lab Test - MRI CT 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 water 3. Place an eye part on the eye for Diplopia 4. 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 day 6. Encourage independence 7. Assist the client to establish a regular exercise and rest program 8. Instruct the client to balance moderate activity with rest periods 9. Assess the need for and provide assistive devices (walker, canes, wheel chair) 10. Initiate physical and speech therapy 11. Instruct the client to avoid fatigue, stress, infection, overheating and chilling 12. 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 muscles that 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 cells Thymus gland o H shaped bi-lobe organ in the root of the neck and in front of the heart o Contains myoid cells which has surface acetylcholine receptors o Infections or inflammatory conditions of the thymus gland may cause production of anti 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 swallowing C. Due to the involvement of the diaphragm and intercostal muscles - Respiratory difficulty decreased vital capacity and tidal volume can lead to respiratory arrest/distress D. Due to spinal accessory nerve/skeletal muscle involvement - Weakness of the neck and muscles cant 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 effect Edrophonium 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 done 4. Cranial Nerve Testing - Cranial nerves are affected in MS 5. 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 PRBC is 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 Management Thymectomy 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 receptor Myasthenic Crisis - Ss Myasthenic Crisis Cholinergic Crisis Insufficiency (Anti-cholinesterase drug under Overdosage of Anticholinesterase dosage/Cholinergic drugs) Increased level of Ach Decreased level of acetylcholine Increase BP Tachycardia Restlessness Apprehension Increase 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 Decreased BO Bradycardia Fasciculation Abdominal Cramping
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Neuro Nursing Ms. Jean Javier

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 suction 2. Instruct client to sit upright when eating 3. Provide ventilator support 4. Plan activities carefully including rest periods. 5. Provide client and family information about MG and treatment including adverse reactions of medication 6. Explain how to recognize myasthenic and cholinergic crises and how to plan for medical help 7. 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, Cephalocaudal Parkinsons 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, stabilization, adjustment 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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Neuro Nursing Ms. Jean Javier

Causes a. Unknown genetic extra copy of a normal gene (SNCA) Alpha sinuclein causes too much build up of protein in the brain - Gene Parkin responsible for the degradation of some of the neuronal proteins releasing free radicals; 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 drying products 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, Thioridazine f. Oral Contraceptives contain estrogen hormone causing increased blood viscosity thrombus formation less blood supply g. Viral infection may attack the basal ganglia h. Diabetes Mellitus peripheral circulation impaired decrease glucose to the brain affecting the basal ganglia Clinical Manifestation Six Cardinal Signs: 1. Tremors at rest common early sign 2. Rigidity general feeling of stiffness 3. Bradykinesia/Akinesia 4. Flexed posture of the neck, trunk and limbs shuffling, propulsive gait 5. Loss of postural reflexes 6. 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 facies Parkinsons 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 Curative 1. Anti-Parkinsonian Agents (Dopaminergic) - Improves muscle flexibility a. Levodopa o Increased levels of dopamine in the brain o Relieves tremors, rigidity and Bradykinesia - S/E: o Anorexia o N and V o Postural Hypotension o Mental changes such as confusion, agitation and hallucination o Avoid multivitamin preparation containing B6, Pyridoxine, and foods high in Vit. B6 blocks desired action of Levodopa (tuna, pork, dried beans, salmon, beef, and liver. o Administer with food or snack to avoid GI irritation o Inform the client that the urine and sweat will be darkened b. Sinemet o Carbidopa with Levodopa o 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 behavior 2. Dopamine Agonists/Antiviral - Dopamine receptor agonists a. Amantadine HCl (Symmetrel) o Blocks the reuptake of dopamine at the synaptic cleft b. 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 for metabolizing 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 discontinued 6. Antihistamine - Diphenhydramine (Benadryl) to decrease tremors and anxiety 7. Antidepressants to improve mode since serotonin levels is decreased - Chlordiazepoxide (Librium) 8. Physical Rehabilitation - May develop contracture 9. Surgery a. 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 rigidity b. Thalamotomy c. Deep Brain Stimulation placement of electrodes in the thalamus then attaching to a pulse generator implanted in the intraclavicular region to relieve tremors d. Experimental Adrenal tissue transplant implantation of adrenal medullary tissue into the corpus striatum to reestablish 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 speak 5. 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 3550g/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 - Administer Laxative (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 task o Lie down on the floor. Relax entire body o Sleep on side that has the tremor - Trouble getting dressed: dress and undress in from of the mirror. Buy clothes with self fastener like Velcro or slide-locking buckles Cerebrovascular Accident WHO Definition: Stroke - A neurological deficit of sudden onset accompanied by focal dysfunction and symptoms lasting more than 24 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 baseline Facts - 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 <10mL/100g of brain/min cell membrane failure occurs: o Inc extracellular K, inc intracellular Ca o Dec ATP, profound cellular acidosis o Cell death o Electrical silence Ischemic Penumbra - The area surrounding the primary injury (necrotic core) - CBF is 10-18mL/100g of brain/min - Electrical silence but irreversible damage has not yet occurred What are the types of stroke? - Ischemic o 85% of strokes o Thrombotic or embolic Ischemic: Thrombotic local origin of clot Usually develops at night during sleep Symptoms perceived in the morning Suspect in history of atherosclerosis, hypercoaguable states (Polycythemia, DIC), and collagen vascular disorders o Ischemic: Embolic proximal origin of clot Occurs at any time Frequently during periods of vigorous activity History of atrial fibrillation, valvular vegetations, thromboembolism from MI, ulcerated plaques in the carotid system o Lack of oxygen caused by cerebral embolism o Caused by thrombosis - Hemorrhagic Stroke o 15% of strokes o Intracerebral > subarachnoid hemorrhage o Occur during stress or excretion o Focal deficits rapidly evolves o Confusion, coma or immediate death o One month mortality
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o 50% for SAH o 80% for intracerebral hemorrhage o More often intracerebral o May occur as a result of aneurysm Premonitory S/Sx 1. Nape pain 2. Severe headache 3. Blurred vision 4. Altered LOC (Confused, light headedness, fleeting loss of consciousness 5. Slurred speech 6. Inc BP 7. 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) Global both 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 Deficits Homonymous 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 Angiography CBC 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. Thrombolytics rtPA Recombinant Tissue Plasminogen Activator - can be given through IV - not given to client with intracerebral hemorrhage Enoxaparin (Clexane) 2. Anticoagulant - In cases of cerebral thrombosis Heparin, Aspirin, Warfarin
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3. Osmotic Diuretic K 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. Laxatives 9. Antifibrinolytic Agent - Epsilon Aminocaproic Acid (Amicar) EACA 10. Antibiotics 11. O2 administration 12. IVF on unaffected side 13. NGT 14. Catheterization 15. Surgery Carotid Endarterectomy - Surgical excision removes atherosclerotic plaques from the inner arterial wall, most commonly the inner 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 prescribed 2. Monitor V/S 3. 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 increased ICP 5. Monitor from increasing ICP because the client is most risk during the first 72 hours following CVA 6. Position the client on the side, with head of bed elevated 15-30 degrees as prescribed 7. 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 bleeding 9. Insert a foley catheter as prescribed 10. Administer intravenous fluids as prescribed 11. Maintain fluid and electrolyte balance 12. 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 swallow 9. Provide sips of fluids and slowly advanced diet to foods that are easy to chew and swallow 10. 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 neck positioned slightly forward and flexed 12. Place food in the back of the mouth on the unaffected side to prevent trapping of food in the affected cheek Intervention in the Chronic Phase of CVA 1. Neglect syndrome a. 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. Hemianopsia a. Client has blindness in the same visual fields b. Homonymous Hemianopsia is blindness in the same visual field of both eyes c. 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 unaffected 4. Place clients personal objects within the visual fields 5. Provide eye care for visual deficits 6. Place a patch over the affected eye if the client has Diplopia 7. Increase mobility as tolerated 8. Encourage fluid intake and a high fiber diet 9. Administer stool softeners as prescribed 10. Encourage client to express feelings
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11. 12. 13. 14. 15. 16.

Encourage independence in activities of daily living Assess the need for assistive devices such as cane, walker, splints, or braces Teach transfer technique from bed to chair and to bed Provide gait training Initiate physical and occupational therapy 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 or shearing force - An insult to the brain that is capable of producing physical, intellectual, emotional, social and vocational changes 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 consciousness 2. Contusion - Bruising injury of the brain o Coup slower moving contents of the cranium strikes bony prominences of dura o 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. Hemorrhage Epidural 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 Subacute Chronic 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. Fracture Types of Skull Fracture 1. Linear Skull Fracture o Single clean break 2. Depressed Skull Fracture o Pushes bony fragments toward the brain 3. Comminuted Skull Fracture o Splinters or crashes skull into many bone fragments 4. Basal Skull Fracture/Basilar skull fractures o 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 contain glucose Halo Sign blood in the center and outside is clear o Periorbital ecchymosis (Raccoons eyes) o Mastoidal ecchymosis (Battles sign) 5. Ethmoid Bone fracture Clinical Manifestation 1. Skull fractures o CSF or other fluid draining from ear or nose o Blood behind tympanic membrane o Periorbital ecchymosis o Bruise over mastoid process o Indication of cranial nerve and inner ear damage o Facial paresis o Vertigo o Nystagmus 2. Concussion o LOC for 5 min or less, transient o Retrograde amnesia can remember the past but not the present o Post traumatic amnesia o Headache, dizziness o N/V o Irritability, lethargy 3. Contusion o Cerebral contusion: Hemiparesis o Brain Stem Contusion Unresponsiveness Coma Cranial nerve dysfunction
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Speech disturbance such as temporary aphasia

Assessment 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 prognosis 2. Respiratory Pattern - It is essential for the nurse to evaluate and record all qualitative characteristics of respiration not just 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) - 3rd 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 Muscle A. Decorticate Rigidity o Cortex of the brain is affected B. Decerebrate o Postural attitude characterized by upper brain stem damage 6. Assess for Rhinorrhea, Otorrhea and Nuchal rigidity Rhinorrhea 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 Eyes 7. Assess for headache, nauseas and vomiting, Diplopia - Monitor V/S reflecting increased ICP or shock (Increased temperature, increased BP, widened pressure, 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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Neuro Nursing Ms. Jean Javier

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 Test X-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. Antibiotics 2. Corticosteroids prednisone 3. Osmotic diuretics 4. Laxatives 5. Vasodilators 6. Antihypertensives 7. Anti-tetanus prophylaxis HTIG; ATS 8. 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

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