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Neuro Lecture Anatomy and Physiology -Neurons-initiate and conduct impulses -Sensory neurons transmit impulses to CNS -Motor neurons transmit impulses away from CNS -Mechanism for nerve impulse conduction -Depolarization; repolarization (Na+, K+, Ca+) Factors affecting nerve impulse transmission: -Distance between neurons -Strength of stimulus or inhibition by another neuron -Inadequate neurotransmitter supply (depression) -Changes in ECF (pH, drugs, ions) -Lack of oxygen (hypoxemia = decreases impulses) -Hypnotics, Anesthetics (inhibit) -Acidosis (decreases rate of impulses) -Alkalosis (excitatory) -Caffeine -Tea (theophilline) -Chocolate Anatomy and Physiology Neurotransmitter: 1

Neuro Lecture notes

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Page 1: Neuro Lecture notes

Neuro Lecture

Anatomy and Physiology-Neurons-initiate and conduct impulses

-Sensory neurons transmit impulses to CNS-Motor neurons transmit impulses away from CNS

-Mechanism for nerve impulse conduction -Depolarization; repolarization (Na+, K+, Ca+)

Factors affecting nerve impulse transmission: -Distance between neurons -Strength of stimulus or inhibition by another neuron-Inadequate neurotransmitter supply (depression)-Changes in ECF (pH, drugs, ions)-Lack of oxygen (hypoxemia = decreases impulses)-Hypnotics, Anesthetics (inhibit)-Acidosis (decreases rate of impulses)-Alkalosis (excitatory)-Caffeine -Tea (theophilline)-Chocolate

Anatomy and PhysiologyNeurotransmitter: -Acetylcholine [ACH – major neurotransmitter of parasympathetic *feed and breed]-Serotonin [inhibitory – sleep, calm, serene]-Dopamine [Catecholamine] (Reward system – sympathetic)-Norepinephrine [Catecholamine]-Amino acids

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-Peptides-Gases [Nitrous]

-Neuroglial cells – four types, provide protection, structure, and nutrition for neurons; part blood brain barrier; assists in regulating composition of CSF-CNS – brain and spinal cord-Cerebral circulation – Circle of Willis-PNS [peripheral nervous system] – spinal nerves, cranial nerves, and autonomic nervous system

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Anatomy and Physiology-ANS – exerts control over “involuntary” functions*Sympathetic – vasodilation in skeletal muscle and vasoconstriction in skin and viscera; increased heart rate and force of contraction; bronchiolar dilation; liver conversion of glycogen into glucose; increased sweat gland activity; decreased peristalsis and gastrointestinal secretions; papillary dilation; thick saliva; hair strands on end; most sympathetic neurons release norepinephrine (from adrenal medulla)

*Parasympathetic – slows heart rate; constricts bronchioles to normal diameter; increases peristalsis and TI secretions; papillary constriction; secretion of thin saliva; normal constriction of bladder; parasympathetic neurons release acetylcholine (digestion)

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Assessment Health Hx: amyotrophic lateral sderosis (ALS), multiple sclerosis (MS), Parkinson’s disease, tumors (glioma, astrocytoma), guillain-barre syndrome, cerebral aneurysm, arteriovenous malformation (AVM), stroke (CVA), migraines, Alzheimer’s disease, myasthenia gravis, congenital defects, metabolic disorder, childhood seizures, diabetes mellitus, pernicious anemia, cancer, infections, thyroid disease, HTN, delivery or child birth event, substance abuse

Neuro AssessmentSurgical Hx: craniotomy, laminectomy, carotid, endarterectomy, transsphenoidal hypophysectomy, cordotomy, aneurysmectomy or repair

Medications: antidepressants, anti-seizure medications, narcotics, anti-anxiety medications

Injuries/Accidents: closed head injuries (CHI), chronic subdural hematoma, spinal cord injury, peripheral nerve damage

Family Health Hx: congenital defects, hydrocephalus, arteriovenous malformations, headaches, epilepsy, Alzheimer’s disease, myelomeningocele, HTN

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Social: ETOH use – Korsakoff’s psychosis, Wernicke’s encephalopathy, polyneruopathy, tremors, tobacco use, drug use – seizures (withdrawal from ETOH, give Ativan) cocaine and meth

General Appearance and Behavior: -Motor activity (disorganized ineffective)-Body posture, position of rest for infant or young child-Dress, hygiene (motor function, use objects)-Facial expression, facial features (Down’s syndrome, Fetal ETOH Syndrome), speech, emotions, stroke, Bell’s Palsy, brain bleed

Communication:-Should be spontaneous, coherent, effortless flow, normal inflections, volume, pitch, articulation, rate and rhythm-Language comprehension should be intact-Ability to read and write should match level of education

Aphasia [communication]Sensory or receptive: inability to understand and interpret oral or written communication Expressive or Broca’s: inability to speak or write, can comprehend speech and written communication (frontal lobe, left side)Mixed: involves both sensory and motor aspects of speech, rarely is aphasia only motor or sensory

Neuro AssessmentLevel of Consciousness (LOC)Eye Opening: open, spontaneous open, open to name, open to tactile stimuli (touch), open to painful stimuli (sternal rub)[state of arousal, reticular activity system; change in LOC signifies trouble]

Glasgow Coma ScaleUsed to evaluate and quantize degree of coma by determining best motor, verbal, and eye opening responses to standardized stimuli (6 motor, 5 verbal, 4 eye)

Eye Opening Response-Spontaneous – open with blinking at baseline 4 points-To verbal stimuli, command, speech 3 points-To pain only (not applied to face) 2 points-No response 1 point

Verbal Responses -Oriented 5 points-Confused conversation, but able to answer questions 4 points-Inappropriate words 3 points-Incomprehensible speech 2 points-No response 1 point

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Motor Responses-Obeys commands for movement 6 points-Purposeful movement to painful stimulus 5 points- Withdraws in response to pain 4 points-Flexion in response to pain (decorticate posturing) 3 points (cortex = flexion)-Extension response in response to pain (decerbrate posturing) 2 points [damage to cerebellum]-No response 1 point

Glasgow Coma ScaleConfusion – GCS = 14Lethargy – GCS = 13 to 14Stupor – GCS = 12 to 13Permanent vegetative state – GCS = 8 to 10Locked-in Syndrome – GCS = 6 (high cervical injury)Coma – GCS = 3 to 6Brain death – GCS = 3

Neuro AssessmentOrientation Person – identifies selfPlace – states town or state, buildingTime – time of day, season, year, month, dateSituation – states current circumstances or current eventInfants and young children – recognize parents

Confusion in the Elderly-Decreased cardiac output (MI, CHF)-Hypoxia (pneumonia)-Neuro (vascular insufficiency, infections, cerebral edema)-Metabolic (increased or decreased sodium, hypo or hyperglycemia, dehydration) -Environmental (surroundings, temperature, sensory over load or deprivation) sepsis or hypoxia

Cognitive Abilities and Mentation-Attention -Memory (3 objects)-Judgment (intact frontal lobe)-Spatial perception (can hold a pen?)-Calculation (subtract by 7’s)-Abstract reasoning (hear story – fable – and understand abstract meaning)-Thought process and content (logical and reality based)

SensoryExteroceptive Sensation: light touch, superficial pain, temperature

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Peroprioceptive Sensation: motion, position, vibration (how to sit in chair correctly, not on head)Cortical Sensation: stereognosis, two point discrimination, extinction (ability to identify object)

Respiratory PatternsRate, Depth, and Rhythms-Bradypnea (depress CNS)-Apnea (brain death)-Cheyne – Stokes (brain stem problems, rapid apnea, rapid – but has a rhythm)-Biot’s or Ataxic – random pattern-Apneustic (timing of inspiration, except not normal)-Neurogenic hyperventilation (panting)-Agonal (guppy fish breathing, only mouth breathing)

Eyes-Oculomtor, CN III, pupils, EOM/Trochlear, CN IV, EOM/Abducens, CN VI, EOM/Acoustic, CN VIII, nystagmus-Position of pupils at rest (conjugate [seated together], disconjuaged [don’t line up])-Eye movements: nystagmus (constant involuntary movement of eyeball), oculocephalic (Doll’s eyes)Equality of pupils – size and shape-Anisocoria (one pupil bigger than other)-Ipsilateral dilatation (one pupil bigger and pupil sluggish)-Pin point (drugs)-Irregular (cataract sx, lens sx, trauma)Presence of direct light and accommodation reflexes-Sluggish (drugs, ICP)-None (blind, glass eye)-Hippus: constricts to light then appears to rhythmically vacillate in size, midbrain lesion-Marcus Gunn: inappropriate consensual reaction, trauma to optic nerve-Non accommodating: blindness, chemical, trauma, death

AssessmentMotor Function-Face – symmetry, equality of movement (smile), CN VII (facial) strokes -Gag and cough reflexes – present, ability to swallow, ability of infant to suck and swallow, CN IX, glossopharyngeal-Movement of Extremities – controlled, to command, no tremors, jerking or twitching-Strength and muscle tone – increased tone (spasticity), decreased tone (flaccid), hemiplegia – loss of function-Babinski reflex – normally negative in adults and children over 1 year of age

These are classic neuro assessment signs…B rudzinski’s sign – flexion of head causes flexion of both thighs at hip joint as well as knee flexion, sign of meningeal irritation Bending of neck

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K ernig’s sign – flexion of thigh and knee to right angles and when extended leads to painful spasm of hamstring Knee already flexed

Motor Function-Seizure activity

Posturing-Decerebrate: extensor posturing, extension and adduction of arms, hyperextension of legs; cerebellum – think like celebrating *worse -Decorticate: flexion posturing, flexion, internal rotation of arms, and extension of legs; cortical – cortex - core-Opisthotonos: position with rigid arching of the back, associated with strychnine poisoning, tetanus, meningitis, epilepsy, rabies; arching can interfere with respiratory muscles -Flaccid posturing: absence of motor activity in any extremity **Worst one to have! From acute spinal cord injury, brain death

Neuro Assessment Vital Signs (Late sign)Blood pressure and pulse changes: Cushing response or reflex – decreased pulse rate (bounding, slow) with increasing systolic blood pressure, widening pulse pressure (norm difference is 40 to 50)Respiratory rate and pattern (there will be a change, brain stem impairment)Temperature: assess in context to overall condition, damage to hypothalamus can lead to neurogenic fever; be sure to rule out infection causing the fever first (hypothalamus)

PainHeadache: increased ICP, brain does not have sensory nerves, pain is d/t compression of arterial walls, veins, and CNs, constant with increasing intensity, aggravated by movementProjectile Vomiting: may occur with nausea, without nausea, unexpected, r/t pressure changes in the craniumInfants: size of fontanel, should match growth and development level, soft with slight pulsations, no bulging or bounding pulsations, approximated cranial suture lines {good final question}

Cranial NervesCN I [Olfaction] – 1st you smell it (have pt smell something)CN II [Optic] – next you see it (Snellen eye chart, newsprint, Rosenbaum’s chart); measure distance, near, and peripheralCN III [Oculomotor] – then you adjust you pupils *typically assessed (to focus on it) want round pupils, responses to light [drug influence – atropine, will dilate pupils]CN III [Oculomotor], CN IV [Trochlear], and CN VI [Abducens] – next you look around (work in conjunction with each other, up, down, side to side

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CN V [Trigeminal] – then you blink (3 branched nerve, motor/sensory/corneal reflex); protect eyes with lube and tape shut; couldn’t not have corneal reflex – drug influenced; trigeminal neuroalgia-very painful, hurts to eat, drink, increased suicide rates from painCN VII [Facial] – then you smile (if cooperate, want to see symmetry – stroke, tumor, can drool and aspirate or even pocket food and protect airwayCN VIII [Acoustic; Cochlear-Vestibular] – then you listen and balance (hearing, vertigo, nystagmus, strabismus); can do Rhine test-measures conduction; Weber test-measures if conduction or nerve issue; Caloric test-vestibular neuro response with water in ear, want to see nystagmus and pt vomitCN IX [Glossopharyngeal] CN X [Vagus] – next you cough, gag, and talk (*manage airway and aspiration, ask pt to cough, tongue depressor – have them say awwwww and look at symmetry of uvula CN XI [Spinal Accessory] – then you shrug your shoulders (against RN’s hands to check strength, symmetry and if equal tone)CN XII [Hypoglossal] – last you stick out you tongue (check midline)

Cerebellar FunctionCoordination – keeps a moving part from overshooting intended target; skilled movements in a sequence; predict distance and speed of approaching object; voluntary control of movement; ipslateral control of side of body

Gait and equilibrium – observe walking and balance; heel to toe walking, Romberg test [where you have pt stand with feet together and close eyes, are they swaying?]

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Reflex ActivityDeep tendon reflexes0: absent reflex [from too much Mag]1+: trace or seen only with reinforcement2+: normal [normal]3+: brisk [normal]4+: nonsustained clonus (eg repetitive vibratory movements)5+: sustained clonus [seizure]…putting pressure on tendon and hammer stretches it

Main Spinal Nerve Roots Involved-Biceps C5, C6-Brachioradialis C6-Triceps C7-Patellar L4

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-Achilles Tendon S1

Cutaneous (skin type) reflexes:-Corneal (CN V and VII) [membrane surface]-Gag (CN IX and X) [cutaneous]-Plantar/Babinski’s sign (CNS) [don’t see in people over 1 year old]-Abdominal reflex (Thoraxic spinal nerves) [T for trunk]-Cremasteric (L1 and L2) [for boys – run something inside the thigh and testes will elevate]-Bulbocavernous (S3 and S4) [for boys – pinch glans penis and scrotum will elevate]-Perianal (S3, S4, and S5) [aka anal wink] may need bowel retraining

Rapid Neurologic Assessment-Glasgow coma scale [assess motor, eye movement and verbal response]-Response to painful stimuli [decreased LOC, do peripheral and central stimuli and see response from client]-LOC-Posture [décor or decereb]-Pupil assessment [PEARLA?]

Laboratory/Diagnostic StudiesFor Each Listed Study:

1. Define and describe2. Explain why it would be done (indications)3. Describe normal and abnormal results [generally speaking]4. Identify client teaching and preparation5. List follow up care including prevention and detection of potential complications

Cushing’s Triad - Cushing's triad is the triad of hypertension (progressively increasing systolic blood pressure), bradycardia and irregular respirations.[1] It is sign of increased intracranial pressure. Other sources state that the triad is hypertension, bradycardia and widening pulse pressure (an increase in the difference between systolic and diastolic pressure over time).

Laboratory/Diagnostic Studies-Blood cultures necessary-CSF analysis-Skull and spine x-ray tests-Cerebral angiography-Myelogram

CT scan: possible use of contrast medium, assess for allergic response, fluids [use of medium contraindicated with hemorrhagic bleed]-Positron emission tomography (PET)-Single photon emission CT (SPECT)-EMG/nerve conduction

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-Evoked potential-MRI/MRA-Transcranial Doppler-Cerebral blood flow -Carotid duplex studies

Lumbar Puncture-Insertion of spinal needle into the subarachnoid space (between the third and fourth lumbar vertebrae)-Contraindicated in clients with increased intracranial pressure-Position-Spinal headache possible from spinal tap

Electroencephalography (EEG)-Graphically records the electrical activity of the cerebral hemispheres-Sleep deprivation requirement-Anticonvulsants possibly withheld

Neurologic (Part I B)HeadachesMigraine headache-Episodic familial d/o manifested by unilateral, frontotemporal, throbbing pain in the head, often worse behind one eye or ear-Often accompanied by a sensitive scalp, anorexia, photophobia, nausea-Aura: sensation that signals the onset of a headache or seizure

Drug therapy-Abortive therapy: alleviating pain during the early aura phase includes prescribing ergotamine derivatives, NSAIDS, triptans, isometheptene combinations-Acetaminophen and NsSAIDs are usually effective for mild migraine headaches

Preventive Therapy-NSAIDS prescription -Beta adrenergic blocker-Ca+ channel blocker

Complementary and alternative therapies-Yoga, meditation, massage, exercise, biofeedback, relaxation techniques-Acupuncture -Use of herbs and nutritional therapies with approval-Avoidance of trigger events that may result in migraine episodes, such as tension and stress

Cluster Headaches-Histamine cephalagia, uncommon type of headache-Cause unknown; attributed to vasoreactivity and oxyhemoglobin desaturation

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-Unilateral, radiating to forehead, temple, or cheek-Ipsilateral tearing of the eye, rhinorrhea, ptosis, and miosis

Therapy-Same types of drugs used for migraines-Client to wear sunglasses and avoid sunlight-Oxygen via mask-Avoidance of precipitating factors, such as anger, excitement-Surgical management

Tension Headache-Neck and shoulder muscle tenderness and bilateral pain at the base of skull and in forehead-Head pain without associated symptoms-Treatment: non-opioid analgesics, muscle relaxants, occasional opioids-Ibuprofen plus caffeine-Prophylactic treatment similar to that used in treating migraine headaches

Seizures and EpilepsySeizure: abnormal, sudden, excessive, uncontrolled electrical discharge of neurons within the brain; may result in alteration in consciousness, motor or sensory ability, and/or behavior [from tumors, brain injury]

Epilepsy: chronic d/o with recurrent, unprovoked seizures; may be caused by abnormality in electrical neuronal activity, and/or imbalance of neurotransmitters (such as GABA) [Gamma amino butric acids which acts as a sedative]

Types of SeizuresGeneralized seizures [impairs consciousness]Absence (petit mal) – lapses of awareness, staring, no warning, no after effect [age 4 to 12, just not there during seizure]Atonic (akinstic, drop attack) – abrupt loss of muscle tone [and loss of consciousness, injury to self, and has resistance to AED [anti epilepsy drug] Myoclonic – rapid, brief contractions of musclesTonic clonic (grand mal) – stiffening of limbs (tonic) [may turn cyanotic], jerking limbs (clonic)*Concerned with injury and airway, describe seizure, find triggers and prevent seizures, and health maintenance

Partial seizures [may or may not lose consciousness]--Simple partial (retained consciousness)--Complex partial (impaired consciousness)Could be sensory or neuro

Status epilepticus – damage to cells with prolong, sporadic chemical messages, want to stop that seizure (Valium)Unclassified seizures

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Types of EpilepsyPrimary or idiopathic epilepsy: not associated with any identifiable brain lesionSecondary epilepsy: results from an underlying brain lesion, most commonly a tumor or trauma [give Dilantin]

Seizures may result from: -Metabolic disorders-Acute ETOH withdrawal-Electrolyte disturbances [increased or decreased Na+]-Heart disease [anoxia, hypoxia, embolus]-Head injuries-Space occupying lesions

Collaborative Management-Complete description of the type of seizure activity that occurs and events surrounding the seizure determines that best treatment plan-Determine whether an aura was present before the seizure in the preictal phase; what was pt doing/what was going on before seizure-Diagnostic testing is performed [may involve inducing seizure]-Manage airway-Describe seizure to HCP

Drug Therapy-Evaluate most current blood level of medication, if appropriate-Dilantin – therapeutic drug level is 10 to 20 mcg/mL; know side effects -Be aware of drug-drug and drug-food interactions-Maintain therapeutic blood levels for maximal effectiveness -Do NOT administer warfarin with Phenytoin (Dilantin with coumadin, they effect each other; Dilantin causes gingival hyperplasia, lowered BP, and sedative effects)-Document and report side and adverse effects

Client and Family Education -Anti-epileptic drugs (AEDs) may not be stopped, even if seizures stop-Refer limited-income clients to social services if have needs-All states prohibit discrimination against people who have epilepsy-Alternative employment may be needed-Vocational rehabilitation my be subsidized

Seizure Precautions-Oxygen and suctioning equipment should be readily available -Saline lock may be necessary [for Ativan or valium]-Side rails should be UP at all times-Padded side rail use is controversial [contraindicated with children]-Place bed in lowest position-Never insert padded tongue blades into the client’s mouth during a seizure

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Seizure Management-If simple partial seizure, observe the client and document the seizure-Turn the client on the side during a generalized tonic-clonic seizure; if possible, turn the client’s head to prevent aspiration-Cyanosis is usually self limiting-Do not restrain

Status Epilepticus Management-Usual causes of status epilepticus:

-Prolonged seizures lasting more than 5 minutes or repeated seizures over the course of 30 minutes-Neurologic emergency that must be treated promptly and aggressively -Sudden withdrawal of AEDs, infections, ETOH withdrawal, head trauma, cerebral edema [from anoxia], and metabolic disturbances (electrolyte imbalances (ammonia), renal failure) [people can seize without movement]

Status Epilepticus Treatment-Establish an airway-Administer oxygen as indicated -Establish IV access-For continuous monitoring, admit client to ICU-Give IV diazepam, lorazepam, Phenytoin, fosphenytoin [like an IV Dilantin – but more compatibility], or general anesthesia-Other treatments include:

-Surgical management: epileptic region in a respectable area-Corpus callostomy – severing the connections between the two halves of the brain-Vagal nerve stimulation

REVIEW REST, CONSIDERED BLOCK 2 STUFF WE SHOULD ALREADY KNOWMeningitis -Inflammation of the arachnoid and pia mater of the brain and spinal cord and the cerebrospinal fluid-Bacterial and viral origins most common: fungal and protozoal meningitis Viral meningitis – self limiting and client recoversBacterial meningitis – a medical emergency with a mortality rate approx 25%

Assessment/Clinical Manifestations-Headache, nausea, vomiting, and fever-Photophobia and indications of increased ICP-Nuchal rigidity: positive Kernig’s and Brudzinski’s signs (only present in 9% of clients)-Seizure, decreased mental status, focal neurologic deficits

Laboratory Assessment of Meningitis -Cerebrospinal fluid analysis

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-Computed tomography scan-Blood cultures-Counterimmunoelectrophoresis-Complete blood count-X – ray study to determine presence of infection

Drug Therapy in Parkinson Disease-Anticholinergic drugs: amantadine, selegilline (confer mild benefit)-Dopamine agonists in the first 3 to 5 years-Levodopa-Bromocriptine or pergolide-Amantadine-Catechol O-methyltransferase inhibitors

Drug Toxicity-Long term drug therapy regimens often cause delirium, cognitive impairment, decreased effectiveness of the drug, or hallucinations-Reduce medication dose-Change medications or frequency of administration-Take “drug holiday”, especially in the use of levodopa therapy

Management of Parkinson Disease-Exercise and ambulation-Self care-Injury prevention -Nutrition -Communication -Psychosocial support-Surgical management includes:

-Stereotactic pallidotomy-Deep brain stimulation-Fetal tissue transplantation

Alzheimer’s Disease -Chronic, progressive, degenerative disease that accounts for 60% of dementias occurring in people older than 65 years of age-Loss of memory, judgment, and visuospatial perception, and changes in personality-Increasing cognitive impairment, severe physical deterioration, death from complications of immobility

Structural Changes -Alzheimer’s disease creates changes that include:

-Neurofibrillary tangles-Senile or neuritic plaques-Granulovascular degeneration -Increased amounts of an abnormal protein, beta amyloid

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-Significantly increased vascular degeneration a contributor to mortality in this d/o-Abnormalities of ACH, norepinephrine, dopamine, and serotonin

Chemical changes in the brain-Alzheimer’s disease creates changes that include abnormalities in the neurotransmitters:

-Acetylcholine-Norepinephrine -Dopamine-Serotonin

-Their exact role is not well understood

Manifestations-Changes in cognition-Alterations in communication and language abilities -Changes in behavior, personality, and judgment-Changes in self care skills-Psychosocial assessment, especially client’s reaction to changes in routine

Interventions in Alzheimer’s disease-Answer client’s questions truthfully -Assess and treat other medical problems-Provide cognitive restructuring and memory training-Structure the environment to increase client’s ability to function-Prevent over stimulation

Interventions-Provide consistency, orientation, and validation therapy -Promote independence in activities of daily living-Promote bowel and bladder continence-Assist with facial recognition as the disease progresses to prosopagnosia, an inability to recognize one self and other familiar faces-Promote communication with clear, short sentences

Drug Therapy-Cholinesterase inhibitors-Memantine-Donepezil-Anti-depressants-Psychotropic drugs-Complementary and alternative therapies

Risk for Injury-Intervention for the client with Alzheimer’s disease: coping with restlessness and wandering; ensuring client wears identification bracelet; registering client in safe return program; providing frequent walks and structured activities

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-Ensuring safety by removing all potentially dangerous objects, particularly in case seizures occur-Minimizing agitation by talking calmly and softly; displaying positive affect; making calm movements; offering diversion

Compromised Family Coping -Interventions for the caregiver’s role:

-Encourage family to seek legal counsel regarding client’s competency, need to obtain guardianship, or durable medical power of attorney, when necessary -Make caregivers and family aware of their own health and stress resulting from new responsibilities for care

Disturbed sleep pattern-Difficulty sleeping at night with frequent naps in the day-Interventions for establishing sleep pattern:

-Re establish the usual day-night pattern by providing activity and exercise during the day-Establish before-bedtime ritual -Adjust treatment and medication schedule to provide for uninterrupted sleep-Give mild anti-anxiety agent or hypnotic

Huntington Disease-Hereditary d/o transmitted as an Autosomal dominant trait at the time of conception -Gradual clinical onset of progressive mental status changes, leading to dementia and choreiform movements in the limbs, trunk, and facial muscles -Three stages each lasting about 5 years over an average 15 years of the disease

Management of Huntington Disease-No known cure or treatment-Genetic counseling -Anti-psychotic agents or monoamine – depleting agents used to manage movement abnormalities that are disabling or interfere with ADL’s -Medication to treat depression, anxiety, and obsessive-compulsive behaviors

Multiple Sclerosis-Chronic autoimmune disease affecting the myelin sheath and conduction pathway of the CNS-Characterized by period of remission and exacerbation -Inflammatory response resulting in random or patchy areas of plaque in the white matter of the CNS

Major Types of Multiple SclerosisRelapsing-remitting – partial or total recovery after attacks; most common formPrimary progressive – progressive from the onset; symptoms generally do no remitSecondary progressive – relapsing remitting course which becomes steadily progressive

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Common Physical AssessmentFindings include: -Flexor spasms at night-Intention tremor-Dysmetria-Blurred vision, dipolpia, decreased visual acuity, nystagmus-Hypalgesia, numbness, tingling or burning-Bowel and bladder dysfunction

Drug Therapy -Biological response modifiers-Immunosuppresives-Steroids-Anti-spasmodics drugs-Adjunctive

Management -Promoting mobility and self care-Managing cognitive problems-Adapting to changes in sexual functioning-Managing bladder and bowel problems-Treating visual disturbances-Complementary and alternative therapies

Amyotrophic Lateral Sclerosis-Known as Lou Gehrig’s disease, a progressive and degenerative disease that involves the motor systemEarly symptoms: fatigue while talking, tongue atrophy, dysphagia, weakness of the hands and arms, fasciculations, nasal quality of speech, dysarthria

Interventions-Riluzole, only drug approved by FDA to extend survival time-Exercise and mobility program (at risk for pneumonia, urosepsis, depression, constipation)-Management of swallowing difficulties -Respiratory support

Guillain-Barre Syndrome -An acute auto immune d/o characterized by varying degrees of motor weakness and paralysis-The client’s life and ultimate potential for rehabilitation dependent upon appropriate interventions and effectiveness of nursing care-Chronic inflammatory demyelinating polyneuropathy Clinical Manifestations-Muscle weakness and pain have abrupt onset; cause remains obscure

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-Cerebral function or papillary signs are not affected -The most common clinical pattern is that the immune system starts to destroy the myelin sheath surrounding the axons-Weakness and Paresthesia being in the lower extremities and progress upward toward the trunk, arms, and cranial nerves in ascending GBS

Ineffective Breathing Pattern Interventions-Priority: maintain adequate respiratory function; implement interdisciplinary actions-Airway management:

*Elevate head of bed at least 45 degrees *Suction

-Chest physiotherapy-Incentive spirometer-Oxygen-Monitor arterial blood gas and vital capacity -Keep equipment for endotracheal intubation at the bedside

Interventions for cardiac dysfunction -Can affect both the sympathetic and parasympathetic systems-Client placed on cardiac monitor because of the risk for arrhythmias -Hypertension treated with beta blocker or nitroprusside-IV fluids for hypotension; client placed in supine position-Atropine may be used for bradycardia

Drug therapy -Plasmapheresis or IV immunoglobin-Plasma exchange-IV immunoglobin

Plasmapheresis -Plasmapheresis removes the circulating antibiotics assumed to cause the disease -Plasma is selectively separated from whole blood; the blood cells are returned to the client without the plasma -Plasma usually replaces itself, or the client is transfused with albumin

Acute Pain Interventions-Assess pain, which is often worse at night -Pain usually only relieved with opiates-Use of analgesia pump or continuous IV drip-Frequent repositioning, massage, ice, heat, relaxation techniques, guided imagery, and distraction (such as music or visitors)

Impaired physical mobility and self care deficitInterventions include:-Assess muscle function every 2 to 4 hours-Provide assistive devices and instructions for their use

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-Ensure safety in ambulation, position changes-Encourage independence-ROM exercises every 2 to 4 hours -Diet plan to guard against malnutrition-Prevention of pressure ulcers-Prevention of pulmonary embolic and DVT

Impaired Verbal Communication Interventions include:-Develop a communication system that meets the needs of client -Devise simple techniques – eye blinking and moving a finger to indicate yes or no responses -Develop a board using letters of the alphabet-Encourage client to verbalize feelings about the illness and its effects-Examine patterns of decision making, roles and responsibilities, and usual coping mechanisms-Refer client to other health care professionals as needed

Myasthenia Gravis-Chronic disease characterized by weakness primarily in muscles innervated by cranial nerves, as well as in skeletal and respiratory muscles-Thymoma: encapsulated thymus gland tumor-Progressive paresis of affected muscle groups that is partially resolved by resting -Most common symptoms: involvement of eye muscles, such as ocular palsies, ptosis, diplopia, weak or incomplete eye closure

Tensilon Testing -Within 30 to 60 sec after injection of Tensilon, most myasthenic clients show marked improvement in muscle tone that lasts 4 to 5 minutes-Prostigmin is also used-Cholinergic crisis is d/t over medication-Myasthenic crisis is d/t under medication -Atropine sulfate is the antidote for Tensilon complications

Diet Therapy and Interventions-Cholinesterase – inhibitor drugs-Immunosuppressants -Corticosteroids for immuno-suppression-Plasmapheresis-Respiratory support-Non surgical management-Assistance with activities and communication

Cholinesterase Inhibitor Drugs-Drugs include anticholinersterase and antimyasthenics

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-Enhance neuromuscular impulse transmission by preventing decrease of Ach by the enzyme ChE-Administer with food -Observe drug interactions

Emergency Crisis-Myasthenic crisis: an exacerbation of the myasthenic symptoms caused by under medication anticholinersterase-Cholinergic crisis: an acute exacerbation of muscle weakness caused by over medication with cholinergic (anticholinersterase) drugs

Myasthenic Emergency Crisis-Tensilon test is performed -Priority for nursing management is to maintain adequate respiratory function-Cholinesterase-inhibiting drugs are with held because they increase respiratory secretions and are usually ineffective for the first few days after the crisis begins

Cholinergic Emergency Crisis- Anticholinergic drugs are withheld while the client is maintained on a vent-Atropine may be given and repeated if necessary -Observe for thickened secretions d/t the drugs-Improvement is usually rapid after appropriate drugs have been given

Management-Immunosuppression-Plasmapheresis-Respiratory support-Promoting self care guidelines-Assisting with communication -Nutritional support-Eye protection-Surgical management usually involving thymectomy

Health Teaching-Factors in exacerbation include infection, stress, surgery, hard physical exercise, sedative, enemas, and strong cathartics-Avoid over heating, crowds, over eating, erratic changes in sleeping habits, or emotional extremes-Teach warning signs-Teach importance of compliance

Polyneruitis and Polyneuropathy-Syndromes whose clinical hallmarks are muscle weakness with or without atrophy; pain that is stabbing, cutting, or searing; Paresthesia or loss of sensation; impaired reflexes; autonomic manifestations-Examples: diabetic neuropathy

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Peripheral Nerve Trauma-Vehicular or sports injury or wounds to the peripheral nerves-Degeneration and retraction of the nerve distal to the injury within 24 hours -Peri operative and post operative care-Rehabilitation through physiotherapy

Restless Legs Syndrome-Leg Paresthesia associated with an irresistible urge to move; commonly associated with peripheral and central nerve damage in the legs and spinal cord-Management: symptomatic, involving treating the underlying cause or contributing factor if known-Non medical treatment-Drug therapy effective for some clients

Trigeminal NeuralgiaAffects trigeminal or 5 th cranial nerve – painful chronic condition affecting one or more branches of the 3 branches of the trigeminal nerve, possibly d/t trauma, infection, degeneration of teeth; other causes include pressure on the trigeminal nerve from a tumor, blood vessel, aneurysm, or multiple sclerosis

Symptoms – clusters of severe, lightening-blot stabs of unilateral facial pain (lips, gums, nose, cheeks); pain may be triggered by brushing teeth, washing face, chewing food, food or fluids of extreme temperatures, clients may be emaciated, depressed, or suffer suicidal ideations

Non-surgical management of facial pain: drug therapySurgical management: micro-vascular decompression, radiofrequency thermal coagulation, precutaneous balloon micro compressionPost operative care: monitoring for complications

Facial paralysis or Bell’s Palsy-Acute paralysis of seventh cranial nerve -Medical management: prednisone, analgesic, antiviral -Protection of the eye-Nutrition -Massage; warm, moist heat; facial exercises

Neurologic Part Two

Stroke/CVA/Brain AttackBrain Attack-A disruption in the normal blood supply to the brain may lead to death after a few minutes-The brain is unable to store oxygen or glucose and must receive a constant flow of blood to function

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-Extent of disability is not known until swelling abates-Return of function – cranial nerve 9 and 10 to assess airway and gag reflex

Types of Strokes-Ischemic strokes [blockage or chunk of stuff]-Thrombotic strokes [plaque from diabetes, smoking, carotid stenosis]-Embolic strokes [a-fib, rheumatic heart dz] -Transient ischemic attack [TIA] and reversible ischemic neurologic deficit [similar to chest for of the heart, can turn permanent]-Hemorrhagic stroke resulting from ruptured aneurysm [head trauma], arteriovenous malformation – tangled mess of veins and arteries, a bulge forms and an aneurysm is made

Health Promotion and Illness Prevention-Avoidance of smoking, sedentary lifestyle, high fat diet-Moderate ETOH consumption [1 oz/day; brain shrivels up and chronic subdural bleeding can occur]-Weight control-Control of HTN [arteries in brain are more delicate, veins don’t have valves – hard to control blood flow]

Neurologic Assessment-Cognitive changes include aphasia [can’t talk], alexia [can’t read], agraphia [can’t write]-Motor changes include hemiplegia [one sided paralysis], hemiparesis [one sided weakness], hypotonia [low tone], flaccid paralysis, hypertonia [spacitiy]

Signs & Symptoms r/t Subarachnoid Hemorrhage -Worst headache of the client’s lifetime **classic sign-Seizures [from bleeding]-Meningeal irritation – nuchal rigidity, positive Kernig sign, positive Brudzinski’s sign [same signs as meningitis]-Changes in LOC, photophobia, incontinence, symptoms of increasing ICP [decreases LOC]-Sensory changes including agnosia [can’t use objects], apraxia [can’t carry out stuff in an organized fashion], neglect syndrome [neglect one side of body], ptosis [droop of eyelid], retinal ischemia causing a brief episode of blindness, hemianopsia [trouble seeing in one visual field]-Perform cranial nerve assessment **-Emotional lability, personality changes, impaired memory, judgment, problem solving, and decision making abilities[right side – goofy, silly, impulsive; left side – agitated, pessimistic]

Drug Therapy- Thrombolytic therapy (systemic or localized) [to treat embolus, thrombus and contraindicated with hemorrhagic]

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-Anti-coagulants, fibrinolytics [ex TPA; onset <3 hrs – will give systemically –OR- >3 hours, will thread cath to the site and give drug there]-Lorazepam and other anti – epileptic drugs [Ativan or Dilantin to prevent seizure]-Ca+ channel blockers [prevent dysfunction of vessels –vasospams-]-Antihypertensives [reduce pressure]-Stool softeners [prevent, reduce strain and bearing down]-Analgesic for pain [reduce pain to help cough and deep breath, but don’t want to mask pain to see what is going on]-Anti anxiety drugs [stress depletes energy that could be going to healing the body]

Complications-with the flow of CSF-Hydrocephalus [water on the brain] – [communicating hydro, when there is not a flow of CSF]; what happens to the pressure in the head when CSF is not able to drain and move as needed – impairs function; txmt – VP shunt to drain fluid from the brain [when just post op, don’t move then up too fast, don’t touch pump, don’t lay pt on pump; if VP shunt becomes infected – s/sx of infection, sepsis, meningitis, etc]-Re-bleeding or rupture – there are windows of time that the pt can re-bleed; 1-2 weeks, there is a high risk of the pt re-bleeding, discharge teaching of pt to contact HCP is there is headache and nausea again-Vasospasms: triple H therapy – damage to structures in the brain, cellular debris causes spasms and loose blood flow distally and loss of consciousness is what happens; keeps pt hyperdynamic – hypervolemic – hypertensive – hemodilution [meaning hyper volume] this is to over come the spasms by cranking up the fluid & Ca+ channel blockers-Seizures – anybody with stuff going on in the cranium is at risk for these

Surgical Management-Carotid angioplasty (most common) – help prevent people from getting ischemia events-Endarterectomy (less safe) – cut open vessel and scrape out junk from vessel-Extracranial – intracranial bypass – by-pass of vessels in veins in the brain

Management of Arteriovenous Malformations-Interventional therapy to occlude abnormal arteries or veins and prevent bleeding from the vascular lesion-Gamma radiation to produce fibrous thickening of the endothelial lining

Management of Cerebral Aneurysms (outpouching of vessels)-Repair via craniotomy (clip, wrap, clamp, add muscle) will wait 3 days until bleeding and edema is under control, then do surgery-Interventional radiology

Management of intracranial bleeding -Craniotomy to remove clots and relieve intracranial pressure [evacuate clot]

Diagnostic Procedures -CT scan [may not show anything in the first scan, may have to wait 24 hours, hemorrhagic will NOT get contrast-

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-SPECT [single photon emission]-MRI/MRA [MRA is more specify to arteries]-Trans cranial Doppler [portable device helps evaluate blood flow, like ultrasound for the brain, looks like altered blood flow, stenosis]-Angiography [sign consent, femoral/carotid artery, assess allergy to dye, hemor – watch closely, assess for s/sx of clot being released and do neuro checks hourly (watch for MI or such)]-CBC, blood glucose, sedimentation rate, PT, PTT, lipid (cholesterol) profile, blood cultures-EKG [a fib or atrial flutter]-Pulse Ox [ensure pt is oxygenated, watch respiratory drive]-Cardiac monitoring -Echocardiogram and/or transesophageal echo [see if there is valve leaflet issues or veggies getting dislodged]

Ineffective tissue perfusion (Cerebral) Interventions-Administer systemic thrombolytic therapy [TPA – have 3 hours]-Perform neurologic assessment-Monitor ICP, assess LOC, elevate the HOB [for most cases, but if somebody has ischemic stroke, might have to lay flat to increase BP [blockage that requires high pressure to get blood around it, HCP will let you know]-Avoid activities and procedures that may increase ICP [hip flexion, valsalva maneuver, sneezing, snug ET tie]-Fully assess need for suctioning [listen, only suction when needed, if it very sensitive they will brady and arterial line will go up]

Impaired Physical Mobility and Self Care DeficitInterventions include:-ROM exercises for the involved extremities -Change of client’s position frequently [as tolerated]-Prevention of DVT -Therapy focused on client performance of ADLs

Disturbed Sensory PerceptionInterventions include:-Right hemisphere [left side neglect syndrome more common with them] damage typically causing difficulty in the performance of visual-perceptual or spatial-perceptual tasks-Activities of daily living-Ambulation-Left hemispheric damage generally causing memory deficits and changes in the ability to carry out simple tasks in a logical manner

Unilateral Neglect-This syndrome is most commonly seen with right cerebral strokeTeach client to:

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-Observe safety measures -Touch and use both sides of the body-Use scanning techniques of turning the head from side to side to expand the visual field

Impaired Verbal Communication-Language or speech problems, usually the result of damage to the dominant hemisphere-Expressive aphasia, the result of damage in Broca’s area of the frontal lobe-Receptive (Weirnicke’s or sensory) aphasia, d/t injury in the temporparietal area

Impaired Swallowing Interventions include:-Assessment of client’s ability to swallow [CN 9 and 10]-Client positioning to facilitate the process of swallowing before feeding-Appropriate diet for the client, including semi soft foods and fluids (thicken)-Aspiration precautions

Urinary and Bowel Incontinence -Altered LOC may cause incontinence or impaired innervation, or an inability to communicate [assess bowel]-Develop a bladder or bowel training program [timing of toileting, after they eat, take them to the restroom; managing meds and stool softeners]

Traumatic Brain Injury-Result of an external force applied to the head and brain causing disruption of physiologic stability locally, at the point of injury, as well as globally with elevations in ICP and potentially dramatic changes in blood flow within and to the brain

Brain InjuriesBlunt trauma – caused by acceleration, deceleration, and rotational forces (MVA, falls, sports, physical assault) [brain hitting the inside of the cranium]Penetrating Injuries – damage to brain and support tissues from piercing forces that transverse skull, projectiles [entered the brain tissue, bullets aka projectiles]Shock wave injuries – like shaken baby issue

Brain Injuries-Process which begins at time of initial insult and may last days to weeks -Neuronal damage consists of neuro-excitation which activates neurotransmitters resulting in depolarization of neurons, aberrant cell signaling (seizures), as well as long term to permanent dysfunction [like a self toxic cycle, keep it calm and not stimulated]-Neuro-filament destruction leads to edema [inflammatory response] and retraction of the axon, eventually permanent destruction of neuron results

Open Head Injuries Linear fracture – simple clean break; the impacted area of bone bends inward and the area around it bends outward

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Depressed fracture – bone is pressed inward into the brain tissue to at least the thickness of the skull [clean, debrided and put on antibiotics] Comminuted fracture – involves fragmentation of the bone, with depression of bone into brain tissueOpen fracture – scalp is lacerated, creating a direct opening to brain tissue

Basilar Skull Fracture-Occurs at the base of skull -Usually extends into the anterior, middle, or posterior fossae and results in cerebrospinal fluid leakage from the nose or ears [CSF may leak, anterior CSF may come from nose rhiorhia, otoria – CSF leaking from ear]-Potential for hemorrhage, damage to cranial nerves, and infection [can find out what CN is damaged by neuro assessment; infection because pathogens can get into fracture]

Types of Closed Head Injuries [based on s/sx]Mild concussion – no loss of consciousness; possible disorientation and confusionModerate concussion – transient focal neurologic deficits with brief loss of consciousnessSevere concussion – prolonged loss of consciousness with neurologic deficit lasting < 24 hours [assess for skull fracture, hematoma, bleeds]

Diffuse axonal injury – can be mild to severe; diffuse areas of white mater have been sheared; evolves over time and may not be apparent on initial CT scanContusion (coup [initial injury like MVA-when brain hits first time] and countercoup [bounces back and hits other part of brain] injury) – brain bruising associated with lacerations/tearing and capillary hemorrhages – can occur with subdural or extraduaral collections of blood [evacuate out hematoma]Rotational – force impacting head with transfer of energy in a non-linear fashion; boxing injury causing shearing and tearing of axons [boxing injuries]

Brain Injuries-Classified according to Glasgow coma scale Severe GCS < or = 8Moderate GCS 9-12Mild GCS 13-15

Brain Injury/ComplicationsImmediate – cerebral bleeding, hematomas, IICP, infection, inflammation, seizures Secondary – 90% of individuals who die after head trauma die from SBI that may occur within minutes of the initial injury [preventing secondary issues and monitoring for additional problems from initial injury]Residual – ex changes in personality or behavior, cranial nerve damage; dependent on area and extent of injury [discharge teaching to family, they will be different – impulsive]

Increased Intracranial Pressure (IICP)

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-An increase in IICP occurs any time there is an increase in the size of intracranial contents; results in progressive neurologic deterioration; specific deficiencies r/t area of brain tissue compression -The cranial vault is rigid with minimal area for expansion of intracranial components[anytime there is an increase in pressure, volume in the cranial vault, there is a change in neuro]

Risk Factors for IICP-Cerebral edema secondary to initial damage; brain tumors, intracranial hemorrhage d/t Closed Head Injury and/or ruptured vessels, cerebralembolism, cerebral thrombosis, hydrocephalus, Reyes syndrome [combination with viral infection and ASA, liver failure, increased ammonia and swelling of the brain]

Monroe-Kelli Hypothesis/Intracranial Pressure Dynamics-Increased in volume of any one component (brain, blood CSF) necessitates reciprocal change in other components [arteries are thinner and veins don’t have vavles; adaptive capacity]-Herniation results when intracranial pressure dynamics are impaired

*Tentorium [posterior, under tentorium, have to cut neck muscles, lay flat]; don’t lay them on the site of the craniotomy, keep them off of incision]

Secondary Responses and Insults-Increased ICP-Hypoxemia [make ICP worse]-Hypercapnia [elevated CO2 levels, vasodilation] will hyperventilate them on purpose on a vent, to prevent buildup of CO2-Systemic hypotension-Infections, encephalitis, meningitis-Cerebral edema

-Cytotoxic [issue with cells themselves]-Vasogenic [bleeding and leakage which increases edema]-Interstitial [in between the cells]

-Hemorrhage-Epidural [usually arterial bleed, quick bleed = quick change in LOC and lose consciousness right away, wake up, lose it again] neurological emergency; arterial between skull and dura mater-Subdural [bleed under dura and above arachnoid, bleeds tends to be venous, drinker, older pt, can have chronic subdurals]-Intra-cerebral [right into brain tissue]

-Hematoma development [that have to be evaluated]-Hydrocephalus-Impaired cerebral auto-regulation-Cerebral Salt Wasting Syndrome [etiology unknown, self limiting, pt can’t hang on to salt, dangerously low amount of Na+; 3% Na+Cl] prone to change in LOC and seizures, will go away in about 2 weeks

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-DI or SIADH [pituitary damage, ADH at risk for dehydration, give desmopressin] [SIADH – too much fluids, diuretics]

Epidural Hematoma-Neurologic emergencies with potentially catastrophic ICP elevation -Arterial bleeding into space between the dura and inner table of skull-Temporal bone fractures, middle meningeal artery-Momentary unconsciousness follows lucid interval within minutes of injury

Subdural Hematoma-Venous bleeding into the space beneath dura and above arachnoid-Most commonly from a tearing of the bridging veins within the cerebral hemispheres or from a laceration of brain tissue-Bleeding occurs more slowly than with a epidural hematoma

Health Promotion/Illness Prevention-Avoid driving while drinking-Follow the game rules cautiously in sports and games-Avoid vehicular speeding-Wear helmet and other protective gear-Avoid dangerous risk taking activities that require training

Assessment -Airway and breathing pattern assessment-Vital signs assessments: Cushing reflex [late sign, slow-bound-full pulse], severe hypertension, widened pulse pressure, and bradycardia-Neurologic assessment *****-Eye assessment [is there pressure on the ocular motor nerve]-Motor assessment [following commands] of posturing

Additional Neurologic Assessment-Assess client’s speech [can they speak?]-Papiledema (choked disc) [HCP checks and do eye exam and can actually see pressure]-Headache and seizure-Leakage of fluid from ears and nose, “halo” sign [or check for glucose]-Nuchal rigidity-Psychosocial assessmentMAP greater than 90 mmHGIntra-cranial pressure ICP <20 mmHgPerfusion pressure 60-100 mmHg

Non-surgical Management of Head Injury-Assessment of vital signs (normotension, mild hypothermia)-Cooling blanket because it decreases metabolism-Pulmonary ventilation and management of oxygen and carbon dioxide levels (normocapnia to mild hypocapnia, oxygenation)

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-Secure airway, maintain patency-Chest physiotherapy, turning as tolerated

Positioning-AVOID pt positions which contribute to increased ICP:-Neck in flexion, extension or misalignment -Knee/hip flexion-HOB flat when ICP elevated [depends on situation]-Completely flat not usually-Trendelenberg [don’t ever do this position]-Pressure of endotracheal/tracheostomy ties on neck veins-Note: If spine clearance has not been determined, consult with MD for pt positioning

Drug Therapy -Glucocorticoids [not really used anymore]-Mannitol [increase LOC, osmotic diuretic so monitor Na+ (osmolarity)], furosemide [take off fluid]-Opioids [calm pt], naloxone [narcan to reverse depression or opioid OD]-Neuromuscular blocking agents [watch joints and movement, mechanical vent, monitor amount of paralysis, neurostimulator]-Anti-epileptic drugs [high % of people with Dilantin {be aware of levels and s/e}-Acetaminophen and aspirin-Barbiturate coma [induced coma using a barb with neuromuscular blocker]

Surgical Management-ICP monitoring devices:

-Intraventricular catheter (IVC) [to drain CSF]-Subarachnoid screw or bolt [does not drain off CSF]-Epidural catheter-Subdural catheter

CSF – ICP – CPPCSF clear, colorless, odorlessICP <20 mmHgCPP 60-100 mmHg in adult

>60 mmHg in child (> 1 year old)>50 mmHg in infant (0-12 months)

CPP = MAP – ICPMAP = (2 diastolic + systolic) divided by 3*Having a P2 higher than a P1 on an ICP is a very bad thing.P1-arterial P2-bounce back of brain tissue, compliance of brain tissueP3-venous pulse wave

Surgical Management -Craniotomy, evacuation VP shunt, loebectomy, gamma knife, bone flap

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-Craniotomy may be performed in extreme instances of elevated ICP; bone flap [can be put in abdomen [mini laparotomy], histology – freeze it, storage fee

Brain TumorsBrain tumors can arise anywhere within the brain structures:-Primary tumors originate within CNS and there will be a neuro change-Secondary tumors result from metastasis in other parts of the body*We will see them post op and have a specific post op assessment

Tumors can lead to cerebral edema, brain tissue inflammation, increased ICP, focal neurologic deficits, obstruction of cerebrospinal fluid flow [hydrocephalus], pituitary dysfunction [common thing]

Classification of Tumors-Malignant or benign-Tumor’s location places it in a class of supratentorial or infratentorial -Tumor’s anatomic origins place it in a class of cellular, histologic, or anatomic

Types of Tumors-Gliomas: malignant-Meningoimas, which arise from the coverings of the brain-Pituitary tumors-Acoustic neuromas, which arise from the sheath of Schwann cells-Metastatic or secondary tumors

Non-surgical Management-Radiation therapy-Chemotherapy-Analgesics-Dexamethasone [type of steroid, used for CNS issues and decrease infla

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-Phenytoin-Ranitidine hydrochloride-Radiosurgery-Zantac

Surgical Management-Craniotomy more often usedPost operative care – positioning, monitoring the dressing, monitoring laboratory values, ventilating the clientDrug therapy – AED, proton pump inhibitors, histamine blockers, corticosteroids, analgesics, acetaminophen, prophylactic antibiotics

Post operative Complications-IICP-Hematomas [secondary]-Hydrocephalus-Respiratory problems-Wound infection-Meningitis -Fluid and electrolyte imbalances [cerebral salt wasting syndrome, DI, SIADH]

Neurologic Part Two B

Back Pain -Low back-Herniated nucleus pulposusPhysical assessment: continuous acute pain, altered gait, vertebral alignment, Paresthesia-Diagnostic assessment using MRI, CT, and electromyography

Non Surgical Management-Williams position, firm mattress or back board under soft mattress; semi fowlers with knees bent-Exercise -Drug therapy-Heat and ice therapy-Diet therapy-Other pain relief measures -Complementary and alternative therapies-Pre-cutaneous laser disk decompression (PLDD)

Surgical Management-Diskectomy-Laminectomy-Spinal fusion (arthrodesis)-Minimally invasive lumbar procedures, such as pre cutaneous lumbar diskectomy, microdiskectomy, laser-assisted laparoscopic lumbar diskectomy

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Post operative Care-Prevention and assessment of complications-Neurologic assessment; vital signs-Client’s ability to void-Pain control-Wound care (prevent infection, monitor for CSF drainage, manage drains)-Client positioning and mobility (log-rolling, brace, avoid twisting)

Cervical Neck Pain -Conservative treatment is the same as described for back pain except that the exercises focus on shoulder and neck-If these treatments do not work, soft collar may be used at night for a period of no longer than 10 days-If conservative treatment is ineffective, surgery such as an anterior cervical diskectomy and fusion is commonly performed

Spinal Cord Injury-Hyper flexion injury MVA-Hyper extension injury MVA-Axial loading injury such as those that occur in jumping-Rotation of the head beyond its range-Penetration injury, such as those wounds caused by a bullet or a knife

Stable – fractures are unlikely to cause further damage and may be treated non-surgically Unstable – spine may need to be surgically realigned and fixed in position to prevent further movement of the vertebrae and further injury to the spinal cord*assume unstable until proven otherwise

Spinal Cord SyndromeAnterior cord syndrome – usually a result of compression of the artery that runs along the front of the spinal cord; compression may be from bone fragments or a large disc herniation [vascular issue]-Patients with anterior spinal cord syndrome usually have complete loss of strength below the level of injury; sensory loss is incomplete; generally, sensitivity to pain and temperature are lost while sensitivity to vibration (tested with a turning fork) and position are preserved Posterior cord lesion – damage towards the back of the spinal cord; may have good muscle power, pain and temperature sensation, however may experience difficulty in coordinating movement of limbsBrown – Sequard syndrome – results in weakness or paralysis (hemiparaphelgia) on one side of the body and a loss of sensation (hemianesthesia) on the opposite sideCentral cord syndrome – incomplete spinal cord injury (in which some of the signals from the brain to the body are not received), characterized by impairment in the arms and hands and, to a lesser extent, in the legs

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Initial assessment-Assessment of the respiratory pattern and ensuring an adequate airway [airway patent]-Assessment for indications of intra-abdominal hemorrhage or hemorrhage or bleeding around fracture sites-Assessment of LOC using Glasgow coma scale

Establish level of injury: Tetraplegia (quadriplegia) –risk for resp [around first vert]Quadriparesis – weakness in all 4 limbsParaplegia – paralysis of legsParaparesis – weakness in legs

The American Spinal Injury Association recommends use of the following scale of findings for the assessment of motor strength in SCI:0 = no contraction or movement1 = minimal movement2 = active movement, but no against gravity3 = active movement against gravity4 = active movement against resistance 5 = active movement against full resistance

C1 to C3 Injuries-Limited head and neck movement; quadriplegia-At risk for autonomic dysreflexia -Electric W/C with “sip and puff” controller-Ventilator dependent – cant’ control diaphragm; at risk for pneumonia, decubes -Requires assistance with all ADLs

-Communication – computer operated using iris recognition, mouth stick or voice recognition, telephone using headset and voice recognition

Cervical InjuriesC4 injuries – similar results as C1-C3 injuries except full movement of head and neck with some shoulder movement *breathe no more*C5 injuries – similar to C1-C4, however may be able to breath without mechanical ventilation C6 injuries – similar results as C1-C5, buy may have weak passive hand grip *ability to use hands*

C7-C8 Injuries -Movement of head, neck, shoulders, partial finger movement, elbow and wrist extension and flexion-Risk for autonomic dysreflexia -Electric or manual w/c-Transfer independently -Drive car with adapted controls

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-Self feeding, self management of bowel and bladder-Requires partial assistance with ADLs and home maintenance

T1-T4 Paraplegia-Full use of head, neck, shoulders, arms, wrists, and fingers-At risk for autonomic dysreflexia-Electric or manual w/c-Independent transfers-Drive a care with hand controls-Self feeding, independent with personal care-Partial assistance needed for home maintenance

T5-T9 Paraplegia -Function similar to T1-T4 injuries -T5 and above associated with GI complications (hypomotility, paralytic ileus, ulcers)-T6 and above associated with autonomic dysreflexia – life threatening ; don’t poop bricks [constipated and have a T6 spine injury]

T10-L1 Paraplegia-Partial paralysis of lower body and legs-Manual wheel chair, independent transfer, may be able to transfer from sitting to standing-Drive hand control adapted care-Self care independent in absence of other factors (additional injuries, severe spasticity- can impair imobility)

L2-L5 Injuries [Cauda equine]-Limited movement of hips, knees, and feet-Manual w/c, independent transfer-May possibly walk with braces and crutches-Drive hand control adapted car-Self care independent in absence of other factors (additional injuries, severe spasticitiy)-S2 & S3 – neurogenic bladder; bladder fx in not normal and not contracting normally

Conus Medullaris and Cauda Equina Syndromes-Lumbosacral injuries is the area of the conus medullaris (T11, T12, L1 – end of the spinal cord) and/or cauda equine (L2-S5)-Variable pattern of motor and/or sensory loss-Commonly results in neurogenic bowel and bladder-Peripheral nerves have the potential for recovery and re-growth

Spinal Shock [serious condition]Characterized by: loss of CNS enervation with the body; deals with tone-Flaccid paralysis-Loss of reflex activity below the level of the lesion (DTRs and cutaneous) [absent deep tendon reflex = DTR, sluggish GI system]

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-Bradycardia [or tachy]-Paralytic ileus -Hypotension [fluid volume may be fine, but leaks out of vessels and fluid goes everywhere]*Can last for months, pt will start to have reflexes return like DTRsT6 and above after spinal shock, at risk for autonomic dysrelexia

Cardiovascular Assessment-Cardiovascular dysfunction is usually the result of disruption of the autonomic nervous system-Bradycardia, hypotension, and hypothermia result from a loss of sympathetic input and may lead to cardiac dysrhythmias-Systolic BP lower than 90 mmHg (may have MAP < 70 mmHg) requires treatment because lack of perfusion to the spinal cord worsens the condition

Autonomic Dysflexia or Hyper reflexia-Life threatening condition that can occur in a person with a T6 or higher spinal cord injury (SCI)-Risk begins after the end of spinal shock-Requires immediate treatment-Massive sympathetic nervous system stimulation

Autonomic Dysreflexia S/Sx-Increased BP greater than 20 mmHg above baseline: BP can reach as high as 330/160-Severe pounding headache [hemorrhage, stroke out]-Diaphoresis and flushing above the level of the SCI-Bradycardia (10% of cases) or tachy-Pallor and gooseflesh below the level of the SCI-Red and sweaty-Anxiety-Visual changes-Nasal congestion-Bronchospasm or respiratory distress-Mydriassi (abnormal dilation of the pupil)-Cardiac irregularities-Patchy erythema above the level of the SCI-Metallic taste in the mouth

Potential Precipitating Factors of Autonomic Dysreflexia-Urologic (90% of all episodes) bladder distention [UTI, kidney stones, catheterization, diagnostic testing]-Gastrointestinal (second most common cause) [bowel over distention – impaction, constipation] hemorrhoids, acute abdominal pain, digital stimulation, diagnostic testing-Cutaneous [pressure ulcers, burns, sunburns, insect bites, ingrown toe nails, blisters, extreme external changes, dressing changes, spasticity, tight clothing or shoes, contact with hard or sharp objects]

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-Reproductive [menstruation, pregnancy or delivery, sexual intercourse, ejaculation, vaginal infection, epididymitis]-Miscellaneous [pulmonary infarct or embol, DVT, heterotrophic ossification, fracture, drug reaction]

Autonomic dysreflexiaTreatment = remove stimulus-High Fowlers position-Loosen any constrictive clothing or devices-Assess bladder and bowel for distention -Un-kink/un-clog indwelling urinary cath-Perform fecal dis-impaction-Administer anti-HTN agent-Cardiac arrest

SCI Assessment-Respiratory and have airway-Gastrointestinal and genitourinary-Musculoskeletal-Psychosocial -Laboratory-Radio graphic and other diagnostic procedures

Ineffective Tissue Perfusion Interventions-Reduction and immobilization of the fracture to prevent further damage to the spinal cord from bone fragment-Non surgical techniques, such as traction or external fixation, but surgery may be necessary

Immobilization for Cervical Injuries-Fixed skeletal traction to realign the vertebrae, facilitate bone healing, and prevent further injuries -Halo fixation – skin break down, center of gravity-Cervical tongs-Pin site care and monitoring of traction ropes-Stryker frame, rotation bed, kinetic treatment table

Halo FixationPin site assessment – erythema, edema, pain, purulent drainageAssess skin under vest daily – erythema, abrasion, irritation; may be necessary to use a flashlight to visualize the skin under the vestNotify MD immediately: if pt reports of feeling head is not secure, any head movement, purulent drainage, erythema, or pain at pin site, fever, change in neuro assessment

Emergency measures: cardiac/respiratory emergency/arrest

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Have RN/MD provide C-spine control/alignment at all times during codeSlide CPR board under pt or use CPR mode on bed (if available)Disconnect vest from halo ring using halo wrench and remove vest

Immobilization of Thoracic and Lumbo-sacral Injuries-Thoracic injuries – bed rest and possible immobilization with a fiber glass or plastic body cast-Lumbar and sacral injuries – immobilization of the spine with a brace or corset worn when the client is out of bed; custom fit thoracic lumbar sacral orthoses preferred

Drug Therapy -Methylprednisolone (controversial)-Dextran – plasma expander, promotes perfusion-Atropine sulfate – for symptomatic bradycardia -Dopamine hydrochloride, Neo-synephrine – for HoTN-Naloxone and TRH – improves spinal cord blood flow-Dantrolene – muscle relaxant-Baclofen – antispasmodic-Etridronate disodium – regulates bone metabolism; treatment for over growth-4-AP K+ channel blocker – experimental – may improve nerve conduction

Surgical Management-Emergency surgery necessary for spinal cord decompression-Decompressive therapy -Spinal fusion-Harrington rods to stabilize thoracic spinal injuries

Ineffective Airway Clearance and Breathing PatternInterventions for client with spinal cord injury:-Airway management is the priority-Clients with injuries at or above the 6th thoracic vertebrae are especially at risk for respiratory complications-Provide measures to maintain airway-Assisted coughing, quad cough, cough assist [abdominal thrust, pushing on abdomen helps loosen those secretions]-Use of incentive spirometer

Impaired Physical Mobility; Self care deficitInterventions include:-In clients with spinal cord injury, monitor for risk of pressure ulcers, contractures, and DVT or PE-Proper positioning, skin inspection, ROM exercise, heparin, and graduated compression stockings-Prevent orthostatic hypotension-Promote self care

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Impairded Urinary Elimination: Constipation-bladder retraining-Spastic bladder: manipulating external area-flaccid bladder: valsalva maneuver -Encouraging consumption of 2000 to 2500 mL of fluid daily to prevent UTI

Long term renal complicationsS/Sx of UTI not perceived by client

Establish a bowel retraining program-consistent time for bowel elimination-high fluid intake for at least 200 ml/day-high fiber diet-rectal stimulation-stool softener

Interventions:-invite clients to ask questions about significant life changes; reply openly and honestly-encourage clients to discuss their perceptions of their situation and copign strategies that can be used-begin a client education program to clarify misconceptions

Spinal Cord Tumor-Surgical management: goal of removing as much of the tumor as possible-Non surgical management: radiation therapy, chemotherapy, pain control

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