Nervous System LECTURE

STRUCTURAL CLASSIFICATION OF THE NERVOUS SYSTEM :
1. CENTRAL NERVOUS SYSTEM Brain Spinal Cord 2. PERIPHERAL NERVOUS SYSTEM Spinal Nerves Cranial Nerves
FUNCTIONAL CLASSIFICATION OF THE NERVOUS SYSTEM :

1. SENSORY or AFFERENT DIVISION Conveys impulses to the CNS Consists of : Somatic Sensory Fibers delivers impulses from the skin, skeletal muscles and joints Visceral Sensory Fibers or Visceral Afferents delivers impulses from the visceral organs
2. MOTOR or EFFERENT DIVISION Carries impulses from the CNS to the effector organs Consists of: Somatic Nervous System or Voluntary Nervous System allows us to consciously or voluntarily control our skeletal muscles Autonomic Nervous System or Involuntary Nervous System regulates events that are automatic or involuntary Sympathetic Nervous System Parasympathetic Nervous System
NEUROTRANSMITTERS :
Acetylcholine used by somatic motor action is inhibited by neurotransmitter inactivated by acetylcholinesterase Catecholamine Neurotransmitters EPINEPHRINE, NOREPINEPHRINE & neurons and its reuptake and is : DOPAMINE, SEROTONIN
these are categorized as MONOAMINES The stimulatory effect of catecholamines are inhibited by: Neurotransmitter reuptake Presynaptic degradation Monoamine Oxidase (MAO) Postsynaptic degradation Catecholamine OMethyltransferase (COMT) Drugs like MAO inhibitors & SSRIs enhance the effect of these neurotransmitters and are thus often used to treat people with depression
NEUROTRANSMITTERS :
Glycine and Gamma-Aminobutyric Acid (GABA)
An inhibitory neurotransmitter, and inhibits the activity of spinal motor neurons thus helping in the control of skeletal movements Acts as a general inhibitory neurotransmitter in the brain, and is often used as a tranquilizer (e.g. the drug : Benzodiazepine Valium ), for mood and emotion disorders
Endorphines & Enkephalins

Helps to block the transmission of pain and also provide pleasant sensations endogenously produced morphine-like substances
CRANIAL NERVES
Name / Number I - Olfactory Composition & Function Sensory - Olfaction
II - Optic
III - Oculomotor
Sensory - Vision
Motor - innervation to the inferior oblique, superior, inferior & medial rectus muscles of the eye Motor eyelid Motor muscles that regulate the lens shape and pupil size Motor superior oblique muscle of the eyeball
IV - Trochlear
CRANIAL NERVES
Name / Number V Trigeminal Opthalmic Nerve Maxillary Nerve Mandibular Nerve VI - Abducens Composition & Function Sensory impulses from cornea, skin of nose, forehead and scalp Sensory impulses from nasal mucosa, upper teeth and gums, palate, upper lip and skin of cheek Sensory muscles of mastication Motor muscles of mastication Motor lateral rectus muscle of the eyeball
CRANIAL NERVES
Motor muscles of facial expression, lacrimal and salivary glands Sensory taste buds of anterior tongue, nasal and palatal sensation VIII - Vestibulocochlear Sensory impulses associated with equilibrium and hearing
IX - Glossopharyngeal Name / Number VII - Facial Composition & Function
Motor muscles of the pharynx that promote swallowing, salivation of parotid gland Sensory taste buds of posterior tongue and carotid artery
Name / Number X - Vagus
Composition & Function

Motor muscles of pharynx (swallowing) and larynx (Phonation) Motor visceral activity: digestive tract and regulates heart rate Sensory taste buds of rear tongue, auricle of the ear and general visceral sensations Motor Laryngeal movement, soft palate Motor & sensory sternocleidomastoid & trapezius muscles
XI - Accessory
XII - Hypoglossal Motor tongue movement Sensory muscles of the tongue
CN
DYSFUNCTION
INTERVENTIONS
I
II
Decreased sense of smell

Decreased visual acuity and visual fields
Is often accompanied by impaired taste and weight loss

Frequent reorientation to environment. Position objects around client in deference to visual impairment Intermittent eye patching Lubricate eyes to protect against corneal abrasions Caution in shaving and mouth care. Choose easy to chew foods with high caloric content. Protect corneas from abrasion by using lubricant Oral hygiene. Account for decreased food intake. Cosmetic approach to hiding facial weakness.
III Double vision (diplopia) IV,V I V Decreased facial sensation Inability to chew Decreased corneal reflexes Facial weakness and decreased taste (anterior tongue)
VII
CN VIII
DYSFUNCTION Hearing loss, imbalance, vertigo, tinnitus
INTERVENTIONS SAFETY! Move slowly to prevent nausea and emesis. Assist ambulation
IX X
XI XII
Dysarthria, Dysphagia, cardiac and respiratory instability

Inability to turn shoulders or turn head from side to side Dysarthria, dysphagia
Maintain airway. Prevent aspiration. Swallow therapy

Mobility aids. Physical therapy Maintain airway. Prevent aspiration. Swallow therapy
SPINAL NERVE PLEXUSES

Plexus Cervical Important Nerves Phrenic Body Areas Served Diaphragm and muscles of the shoulder & neck Deltoid muscle Result if Damaged Respiratory paralysis Paralysis and atrophy of the deltoids Wristdrop inability to extend hand at the wrist Inability to pick up small objects Clawhand inability to spread fingers apart
Brachial
Axillary
Radial
Triceps & extensor muscles of the forearm Flexor muscles of the forearm Wrist & hand muscles
Median
Ulnar
Plexus Lumbar
Important Nerves Femoral
Body Areas Served Lower abdomen, buttocks, anterior thighs and skin of leg and thigh Adductor muscles of thigh and small hip muscles, skin of thigh and the hip joint Lower trunk and posterior surface of the thigh and leg Lateral aspect of leg & foot Posterior aspect of leg & foot
Result if Damaged Inability to extend the leg and flex hip, loss of cutaneous sensation Inability to adduct the thigh
Obturator
Sacral
Sciatic
Inability to extend hip and flex knee Footdrop inability to dorsiflex the foot Inability to plantar flex & invert the foot, shuffling gait
Fibular
Tibial
Plexus Sacral
Important Nerves Superior & Inferior Gluteal
Body Areas Served Gluteus muscles
Result if Damaged Inability to extend the hip (maximus) or abduct and medially rotate the thigh (medius)
AUTONOMIC NERVOUS SYSTEM

Consists of the SYMPATHETIC NERVOUS SYSTEM and the PARASYMPATHETIC NERVOUS SYSTEM
SYMPATHETIC NERVOUS SYSTEM Called the FIGHT or FLIGHT system Also called the ADRENERGIC SYSTEM Four Main Adrenergic receptors: Alpha located in vascular tissues (vessels) of smooth muscles Stimulated: increases force of heart contraction. Vasoconstriction increasing BP. Mydriasis dilates the pupils. Glandular decreases salivary secretion Alpha Inhibits release of norepinephrine dilates blood vessels thus decreasing BP, producing Hypotension
SYMPATHETIC NERVOUS SYSTEM Four Main Adrenergic receptors: Beta located primarily in the heart Stimulated: increases heart rate and force of contraction / myocardial contractility Beta Mostly in the smooth muscles of the lungs, arterioles of skeletal muscles and the uterine muscles Stimulation: bronchodilation, increased blood flow to skeletal muscles and uterine relaxation Other Adrenergic receptors: Dopaminergic Located in renal, mesenteric, coronary and cerebral arteries Stimulated: vessels dilate & blood flow increases
SYMPATHETIC NERVOUS SYSTEM Neurotransmitters used: Epinephrine Norepinephrine Dopamine collectively, these are called Catecholamines PARASYMPATHETIC NERVOUS SYSTEM Neurotransmitter used: Acetylcholine Two Main Adrenergic receptors: Muscarinic Receptors Stimulate smooth muscles and slows down the heart rate Nicotinic Receptors Affects skeletal muscles
EFFECTS OF THE ANS

Organ Eye (iris) Eye (Ciliary muscle) Lacrimal Glands Salivary Glands Sweat Glands Digestive System PSNS Constricts pupils Contraction for vision Production of tears Production of saliva No effect Increased peristalsis and amount of secretion, relaxation of sphincters SNS Dilates Pupils Relaxation for vision Inhibits : dry eyes Decreased : dry mouth Perspiration
near
far
Decreased activity and amount of secretion, constriction of sphincters Hormone secretion Release of Glucose Bronchodilation Increased HR & force of contraction
Adrenals Liver Lungs Heart
No effect No effect Bronchoconstriction Dereased HR, slows and steadies
Organ
PSNS
SNS
Urinary bladder
Kidneys Blood vessels
Relaxes sphincters (allowing voiding) No effect

No effect on most, dilation on a few (penis)
Arrector Pili Muscles

Cellular Metabolism
No effect
No effect
Constricts sphincters (Prevents voiding) Decreased urine production Constricts in viscera and skin / dilates those in skeletal muscles and heart, increased BP Hair erection goosebumps
Increased metabolic rate, increased blood sugar and stimulates fat breakdown Ejaculation Contraction pregnant women in
Penis Uterus
Erection No effect
Technique of objectifying a clients level of responses;clients best response in each area is given a numerical value,and the three values is totaled for a score ranging from 3 - 15. EYE OPENING ABILITY: Spontaneous To voice / speech To pain None
-------------------------------------
(4) (3) (2) (1)
BEST MOTOR RESPONSE - UPPER LIMB: Obeys commands ---------Localizes to pain ---------Flexor withdrawal(decorticate posturing) ---------Abnormal flexion(decerebrate posturing) ---------Extension ---------Flaccid ----------
(6) (5) (4) (3) (2) (1)
BEST VERBAL RESPONSE: Oriented Confused conversation Inappropriate words Incomprehensible sounds None
----------------------------------------------
(5) (4) (3) (2) (1)
A score of 15 indicates client is awake and oriented. A score of 7 - 4 is considered coma. The lowest score is 3,client is considered in deep coma.
SKULL AND SPINAL X-RAY
reveal the size and shape of the skull bones, suture separation in infants, fractures or bony defects, erosion, or calcification identify fractures, dislocation, compression, curvature, erosion, narrowed spinal cord, and degenerative processes
IMPLEMENTATION PREPROCEDURE
immobilization of the neck if a spinal fracture is suspected Remove metal items from body parts If the client has thick and heavy hair, this should be documented, because it may affect interpretation of the x-ray film
COMPUTED TOMOGRAPHY (CT) SCAN
a type of brain scanning that may or may not require an injection of a dye used to detect intracranial bleeding, spaceoccupying lesions, cerebral edema, infarctions, hydrocephalus, cerebral atrophy, and shifts of brain structures
Obtain a consent if a dye is used Assess for allergies to iodine, contrast dyes, or shellfish if a dye is used Instruct the client in the need to lie still and flat during the test Remove objects from the head, such as wigs, barrettes, earrings, and hairpins Assess for claustrophobia
Inform the client if possible mechanical noises as the scanning occurs Inform the client that there may be a hot, flushed sensation and a metallic taste in the mouth when the dye is injected Note that some clients may be given the dye even if they report an allergy, and are treated with an antihistamine and corticosteroids prior to the injection, to reduce the severity of a reaction
IMPLEMENTATION POSTPROCEDURE
Provide replacement fluids because diuresis from the dye is expected Monitor for an allergic reaction to dye Assess dye injection site for bleeding or hematoma, and monitor extremity for color, warmth, and the presence of distal pulses
MAGNETIC RESONANCE IMAGING (MRI)
a noninvasive procedure that identifies types of tissues, tumors, and vascular abnormalities
Similar to the CT scan but provides more detailed pictures and does not expose the client to ionizing radiation
1.
Remove all metal objects from the client Determine if the client has a pacemaker, implanted defibrillator, or metal implants such as a hip prosthesis or vascular clips because these clients cannot have this test performed Instruct the client that he or she will need to remain still during the procedure
2.
3.
1.
client may resume normal activities expect diuresis if a contrast agent was used
2.
LUMBAR PUNCTURE
Insertion of a spinal needle through L3-L4 interspace into the lumbar subarachnoid space to obtain cerebrospinal fluid (CSF), measure CSF fluid or pressure, or instill air, dye or medications Contraindicated in clients with increased intracranial pressure, because the procedure will cause a rapid decrease in pressure within the CSF around the spinal cord, leading to brain herniation
AMERICAN DREAM REVIEW INSTITUTE
obtain a consent have the client empty the bladder
IMPLEMENTATION DURING THE PROCEDURE
position the client in a lateral recumbent position and have the client draw knees up to the abdomen and chin onto the chest Assist with the collection of specimens (label the specimens in sequence) Maintain strict asepsis
Monitor vital signs and neurological signs Position the client flat as prescribed Force fluids Monitor I & O
MYELOGRAM
Injection of dye or air into the subarachnoid space to detect abnormalities of the spinal cord and vertebrae
Obtain a consent Provide hydration for at least 12 hours before the test Assess for allergies to iodine Premedicate for sedation as prescribed
if a water-based dye is used, elevate the head 15 to 30 degrees for 8 hours as prescribed If an oil-based dye is used, keep the client flat 6 to 8 hours as prescribed If air is used, keep the head lower than the trunk as prescribed Assess for bladder distention and voiding
CEREBRAL ANGIOGRAPHY
Injection of contrast through the femoral artery into the carotid arteries to visualize the cerebral arteries and assess for lesions

obtain a consent Assess the client for allergies to iodine and shellfish Encourage hydration for 2 days before the test NPO 4 to 6 hours prior to the test as prescribed Mark the peripheral pulses Remove metal items from the hair
Monitor for swelling in the neck and for difficulty swallowing and notify the physician if these symptoms occur Elevate the head of the bed 15 to 30 degrees only if prescribed Keep the bed flat if the femoral artery is used, as prescribed Assess peripheral pulses Immobilize the puncture site for 12 hours as prescribed Apply sandbags and a pressure dressing to the injection site as prescribed Force fluids
ELECTROENCEPHALOGRAPHY
A graphic recording of the electrical activity of the superficial layers of the cerebral cortex
Wash the clients hair Inform the client that electrodes are attached to the head and that electricity does not enter the head Withhold stimulants, antidepressants, tranquilizers, and anticonvulsants for 24 to48 hours prior to the test as prescribed
Wash the clients hair Maintain side rails and safety precautions if the client was sedated
CALORIC TESTING (OCULOVESTIBULAR TESTING)

Provides information about the function of the vestibular portion of the eighth cranial nerve and aids in the diagnosis of cerebellum and brainstem lesions
PROCEDURE

Patency of the external canal is confirmed Cold or warm water is introduced into the external auditory canal Stimulation of the auditory canal with warm water produces a horizontal nystagmus toward the side of the irrigated ear when the vestibular eighth cranial nerve is normal
Stimulation of the auditory canal with cold water produces a horizontal nystagmus away from the side of the irrigated ear if the brainstem is intact
CRANIOTIOMY
NURSING INTERVENTIONS PREOPERATIVE

Routine pre-op care Shampoo the scalp and check for signs of infection Shave hair Evaluate and record baseline vital signs and neuro checks Avoid enemas unless directed (straining increase ICP) Give pre-op steroids as ordered to decrease brain swelling Insert Foley catheter as ordered
NURSING INTERVENTIONS: POSTOPERATIVE
Supratentorial incision elevate head of bed 15-45 degrees as ordered; position on back (if intubated or conscious) or on unaffected side; turn every 2hours to facilitate breathing and venous return Infratentorial incision keep of head flat or elevate 20-30 degrees as ordered; do not flex head on chest; turn side to side every 2 hours using a turning sheet; check respirations closely and report any signs of respiratory distress

watch for signs of diabetes insipidus (severe thirst, polyuria, dehydration) and inappropriate ADH secretion (decreased urine output, hunger, thirst, irritability, decreased LOC, muscle weakness) For infratentorial surgery may be NPO for 24 hours due to possible impaired swallowing and gag reflexes

check dressings for excessive drainage, CSF, infection, displacement, and report to physician if surgical drain is in place, note color, amount, and odor of drainage Administer medications as ordered a. Corticosteroids to decrease cerebral edema b. anticonvulsants to prevent seizures c. stool softeners to prevent straining d. mild analgesics Apply ice to swollen eyelids; lubricate lids and areas around eyes with petrolatum jelly
an increase in intracranial bulk due to an increase in any of the major intracranial components: Brain tissue (1400 g) Blood (75ml) CSF (75ml)
CSF fluid pressure greater than 15 mmHg Common Causes: Head injury Tumors Abscesses Hemorrhage Edema Hydrocephalus inflammation Surgery
Monroe-Kellie hypothesis:
Because of limited space for expansion
in the skull, an increase in any one of the 3 components (Brain, Blood & CSF) causes a change in the volume in the others by: Displacing them or shifting CSF Increasing the absorption of CSF Or decreasing cerebral blood flow
Increased ICP significantly reduces blood flow resulting to ischemia if complete ischemia lasts for 3-5 minutes (6 minutes max), irreversible brain damage occurs
Autoregulation refers to the brains ability to change the diameter of the blood vessels automatically to maintain a constant cerebral blood flow during alterations in systemic blood flow.
Cushings Triad occurs once the brains protective mechanism is no longer effective Bradycardia Hypertension Bradypnea
ICP
if untreated could lead to herniation / displacement of brain tissue & occlusion of cerebral blood flow brain death follows if ischemia and infarction are left untreated
Intracranial pressure may be measured During a Spinal Tap / Lumbar Puncture By directly attaching a device referred to as a bolt to a small hole in the skull Increased intracranial pressure is almost always indicative of severe medical problems. The pressure itself can be responsible for further damage to the CNS by Decreasing blood flow to the brain Causing the brain to herniate (push through) the opening in the back of the skull where the spinal cord is attached (Foramen Magnum) which is Fatal
Signs and symptoms:

Infants: Bulging fontanel High-pitched cry Poor feeding Separated sutures Older children and adults: Change in LOC (earliest sign) Progresses from Restlessness -----> to Confusion -----> to
Disorientation -----> to Lethargy -----> to Stuporous -----> to Coma
Tachypnea (initial manifestation) Widening Pulse Pressure (initial manifestation) Projectile vomiting Headache increasing in intensity, aggravated by movement and straining Changes in behavior Seizures Ipsilateral pupillary dilatation due to compression of C.Nerve III Pupils eventually become fixed and Dilated Setting-Sun Sign (sunset eyes) a late and ominous sign of increased ICP Note: Slow increases are tolerated fairly well in young children before they become symptomatic. Adults tolerate increased ICP less well.
Management:
Establish and maintain a patent airway and provide adequate ventilation Monitor V/S Position: head of bed elevated 30 45% Prevent further increase in ICP Maintain a quiet and comfortable environment Avoid use of restraints Prevent straining stool softeners and laxatives as ordered Prevent vomiting antiemetics Prevent excessive coughing avoid clustering nursing care activities together Prevent complications of immobility
Management:
Medications Osmotic Diuretics (Mannitol Osmitrol) Furosemide (Lasix) Corticosteroids (Dexamethasone Decadron) Anticonvulsants (Phenytoin Dilantin) Analgesics : Small doses of Codeine stronger analgesics are Contraindicated because they cause: Respiratory depression Altered LOC Pupillary changes
Treat fever aggressively increases cerebral blood flow and cerebral blood volume
HYDROCEPHALUS
A condition of altered production, flow, or absorption of cerebrospinal fluid (CSF) Characterized by an abnormal increase in CSF volume within the intracranial cavity and by enlargement of the head in infancy Occurs in approximately 3 to 4 cases per 1,000 births
HYDROCEPHALUS
Two causes:
Decreased
absorption of CSF Overproduction of CSF
Two types: Non-communicating

(obstructive/internal/intraventricular) Obstruction in the system between the CSF production (ventricles) and the area of its reabsorption (subarachnoid space) Causes: congenital malformations, tumors encroaching on the ventricular system, inflammation or hemorrhage
HYDROCEPHALUS
Two types: 1. Non-communicating

(obstructive/internal/intraventricular) Obstruction in the system between the CSF production (ventricles) and the area of its reabsorption (subarachnoid space) Causes: congenital malformations, tumors encroaching on the ventricular system, inflammation or hemorrhage May be partial, intermittent, or complete Occurs in majority of cases
HYDROCEPHALUS
Two types:
2.
Communicating (extraventricular) Results from impaired reabsorption of CSF from the arachnoid villi into the venous system or excessive production of CSF Causes: SAH, developmental malformation, head injury, neoplasm
HYDROCEPHALUS
Pathophysiology Ventricular system becomes greatly enlarged as well as the cerebral hemispheres, gyri become less prominent, white matter is reduced in volume Increased ICP is determined by fluid accumulation and type of hydrocephalus, age at onset, rapidity and extent of pressure rise
HYDROCEPHALUS
Acute hydrocephalus usually seen in head injury, related to increased ICP Slowly developing hydrocephalus may not cause IICP but produce progressive dementia, and gait changes
HYDROCEPHALUS
Clinical Manifestations
Hydrocephalus in utero or infancy or before cranial suture fusion

Expansion of the ventricles, cranial sutures separate, head expands, and bulging of fontanels Increased ICP to a lesser as the head is able to expand Alteration in muscle tone including clonus and spasticity Scalp with prominent scalp veins, sunset eyes as infant cannot gaze upward Strabismus, nystagmus, optic atrophy Infant has difficulty holdig head up Child may experience physical or mental devt. lag
HYDROCEPHALUS
Clinical Manifestations Hydrocephalus in older children and adults Head does not expand leading to signs of increased ICP: headache, vomiting, papilledema, mental deterioration Declining memory , apathy, inattentiveness, indifference to self and others. Urinary incontinence
HYDROCEPHALUS
Diagnostic Evaluation

Clinical presentations Transillumination of infants head indicates abnormal fluid collection Percussion of infants skull produce a typical cracked pot sound (Macewens sign) Papilledema CT San diagnostic tool of choice Skull x-ray shows widening of fontanelle, sutures, and erosion of intracranial bone
HYDROCEPHALUS
Management
Surgical procedures Direct operation of lesion causing obstruction such as tumors Intracranial shunts for non-communicating hydrocephalus diverts fluid from obstructed segment of ventricular system to the SAS Extracanial shunts most common
HYDROCEPHALUS
Extracranial Shunt procedures Ventriculoperitoneal shunt (V-P shunt) Diverts CSF from a lateral venrticle or spinal SAS to peritoneal cavity Ventriculo-atrial shunt (V-A shunt) diverts CSF to right atrium or superior vena cava Ventriculopleural shunt diverts CSF to pleural cavity Ventriculo-gallbladder shunt diverts CF in common bile duct
HYDROCEPHALUS
Shunt complications Need for shunt revision from occlusion, infection or malfunction Shunt revision from grwoth of child V-A shunt endocardial contusion and clotting bacterial endocarditis, bacteremia, ventriculitis, thromboembolism
HYDROCEPHALUS Complications
Seizures Herniation of brain Spontaneous arrest from neural compensatory mechanism, IICP, and brain herniation Development delays Mental deterioration in adult
HYDROCEPHALUS
Nursing Assessment
Infants: head circumference, fontanelles for tense and bulging, pupilary response, LOC, breathing patterns, emesis, motor, devtal milestones Older child and adult: v/s, sings of IICP, headache, emesis, LOC, motor function, milestones, declining memory , apathy, inattentiveness, indifference to self and others, Urinary incontinence
HYDROCEPHALUS
Nursing Diagnoses
Altered cerebral tissue perfusion related to IICP prior to surgery Altered nutrition: LBR related to reduced oral intake and vomiting Risk for injury related to malfunctioning shunt Risk for infection related bacterial infiltration of the shunt
HYDROCEPHALUS
Nursing Interventions Maintain cerebral tissue perfusion Provide adequate nutrition Maintain skin integrity Reduce anxiety Maintain fluid balance Prevent infection Strengthen family coping
HYDROCEPHALUS
Special consideration Stress importance of resocgnizing s/s of IICP Report shunt malfunction or infection immediately to prevent IICP Regular follow up check ups esp for shunt monitoring
HYDROCEPHALUS
Evaluation
No changes in v/s, LOC, head size, no vomiting, pupils equal and responsive No significant weight loss, stable level of consciousness No skin breakdown Urine intake less than intake, skin turgor normal Afebrile Parents seeking resources
Acute peripheral facial paralysis involving 7th cranial nerve (Facial Nerve) on one side producing weakness of facial muscle Common between age 20 50 Lasts only for 2 8 weeks Etiology : Unknown Viral infection Vascular ischemia Autoimmune disease
CLINICAL MANIFESTATIONS
Majority have upper respiratory infection 13 weeks before the onset of symptoms Distortion of the face Lagopthalmos unable to close the eyes Decrease taste sensation of anterior 2/3 of the tongue Decreased tear production Speech alteration Difficulty Swallowing
MANAGEMENT
Prednisone Protection of the involved eye Artificial tear drops Manually Close eyes if necessary Physical therapy :
application
of moist heat facial massage facial exercise
of the 5th cranial nerve Characterized by sudden paroxysms of sharp, stabbing, excruciating pain in the distribution of one or more branches of the trigeminal nerve Unknown etiology
Condition

Sudden, severe pain on one side Without warning Ends abruptly With pain free interval Precipitated by : Face movement Talking Chewing Yawning Swallowing Shaving Exposure to cold wind
MANAGEMENT

Carbamazepine (Tegretol) Injection of alcohol & ethanol Percutaneous radiofrequency trigeminal gangliolysis low voltage stimulation of the trigeminal nerve by elctrodes which destroys sensory function Microvascular decompression of trigeminal nerve treatment of choice for younger generation willing to accept craniotomy & is the most effective form of treatment Open surgery Rhizotomy (transsection of nerve root)
Any functional abnormality of the CNS when the normal blood supply to the brain is disrupted Impairment could be due to a partial or complete occlusion of a blood vessel or hemorrhage resulting from a tear in the vessel wall
Transient or temporary episode of neurologic dysfunction due to an interruption of blood flow to a focal area in the brain Lasts minutes hours (not longer than 24 hours) Risk Factors: HPN Family History of Stroke DM Atherosclerosis Heart Disease Smoking Obstruction of cerebral microcirculation (Emboli)
Assessment:
Amaurosis Fugax (sudden, painless loss of vision in one eye) Weakness Aphasia Vertigo, diplopia Numbness, paresthesias or ataxia Dysphagia Homonymous Hemianopsia Carotid bruit History of headaches with a duration of days before the attack
Management: Anti-coagulant therapy Platelet aggregation inhibitors - to reduce the incidence of stroke: Aspirin Ticlopidine (Ticlid) Surgical management: carotid endarterectomy Intracranial anastomosis angioplasty Reduce risk factors : Control BP, DM, Hyperlipidemia and Smoking cessation Thrombolytic therapy 3 to 5 hours after onset Streptokinase Recombinant Tissue Plasminogen Activator (rt-PA)
Onset and persistence of neurologic dysfunction lasting longer than 24 hours Results from a disruption of blood supply to the brain
Two Major Categories: 1. Ischemic / Non - hemorrhagic Stroke

Thrombosis Cerebral embolism Ischemia Cerebral hemorrhage (rupture of a blood vessel)
2. Hemorrhagic Stroke
STROKE: RISK FACTORS

Hypertension TIA Heart disease Elevated cholesterol Diabetes Mellitus Obesity Atherosclerosis Carotid bruit Cigarette smoking Sickle cell disease Emboli Sedentary Lifestyle / immobility Stress
Stroke.exe
DIAGNOSTIC EVALUATIONS
CT Scan Cerebral angiography PET Scan CBC with platelet count Lipid profile ECG Chest PA FBS, Serum creatinine, sodium

Sudden, severe headache and nuchal rigidity Sudden numbness or muscle weakness Difficulty of speaking Difficulty of swallowing Impairment of sensation Confusion / change in mental status Parietal Cortex: Hemiparesis occurs on opposite side of the body Temporal Cortex: Difficulty speaking or understanding language or both Occipital Cortex: visual defects (homonymous hemianopsia) Cerebellum: Vertigo, Ataxia Numbness (paresthesia), Weakness (paresis) or loss of motor paralysis (plegia) on one side of the body
Management:
Acute Phase
Maintain patent airway & adequate ventilation V/S observe for signs of increased ICP, shock, hyperthermia and seizures Complete bed rest Maintain F&E imbalance and ensure adequate nutrition
IV therapy for the first few days NGT if unable to swallow Fluid restriction as ordered to decrease cerebral edema
Maintain proper positioning, body alignment & skin integrity:

Elevate head of bed 30 45 degrees to decrease ICP Turn and reposition every 2 hours (only 20 minutes on affected side) Passive ROM every 4 hours Turn client and apply lotion on skin
Maintain adequate elimination:

Offer bedpan and urinal every 2 hours, catheterize only if necessary Stool softeners & laxatives as ordered
Management:
Acute Phase
Provide a quiet and restful environment Medications Osmotic diuretics (Mannitol) & corticosteroids (dexamethasone) to decrease cerebral edema Anticonvulsants (phenytoin Dilantin) Thrombolytics (hemorrhage must be ruled out first) Streptokinase / Urokinase Recombinant Tissue Plasminogen Activator (rt-PA) Anticoagulants (hemorrhage must be ruled out first) Heparin (Antidote: Protamine SO4) Warfarin (Coumadin) : antidote - Vitamin K Aspirin, Ticlopidine (Ticlid) & dipyridamole (Persantine) Antihypertensives for Hypertension Neuroprotectants: Citicholine Piracetam
Management: Rehabilitation
Safety measures Dysphagia Check gag reflex before feeding / upright position Place food on unaffected side of the mouth Offer soft foods Homonymous Hemianopsia can lead to visual neglect Approach client on unaffected side Place personal belongings, food, etc on unaffected side Gradually teach the client to compensate by SCANNING turning head to see things on the unaffected side Emotional lability mood swings / frustration Create a quiet, restful environment Maintain calm, non-threatening manner Explain to family that behavior is not purposeful
Management: Rehabilitation
Aphasia Receptive Aphasia Give simple, slow directions Give one command at a time, gradually shift topics Use non-verbal techniques of communication Speak at normal tone and volume clients hearing is intact Expressive Aphasia Listen and watch carefully when the client speaks Anticipate needs to decrease frustration Allow sufficient time for client to answer, do not press for answers Apraxia loss of ability to perform purposeful skilled acts Guide client thru intended movement Keep repeating the movement
APHASIA

Acquired disorder of communication A general term that encompasses varying degrees of inability to comprehend, integrate, and express language May involve impairment of the ability:

To speak To understand the speech of others To read To write To calculate To understand gestures
APHASIA
Causes Vascular lesion of the cerebral artery especially the dominant hemispheres (left: dominant in 95% of right handed and 70% in left handed individuals) Stroke Head injury Bran tumors Brain cysts
3 Categories of Fluent Aphasia

Wernickes,
receptive aphasia
characterized
by the inability to comprehend the speech of others and of oneself and includes deficits of reading Patient speaks readily but speech lacks clear content, information, and direction, jargon frequently used
Anomic
aphasia (amnesiac aphasia) speech is nearly normal except for difficulty in finding singular words
Marred
by word-finding difficulty
Conductive
(Conduction) aphasia characterized by good comprehension of language but difficulty repeating spoken material
APHASIA
Expressive or non-fluent aphasia

Characterized
by an inability to spontaneously communicate or translate thoughts or ideas into meaningful speech or writing Speech production is limited, effortful, and halting and poorly articulated Comprehension is normal Associated with lesions in Brocas area of the frontal lobe Brocas aphasia
APHASIA
Global aphasia characterized by severe disruption of all aspects of communication including verbal speech, written, reading, understanding.
APHASIA

Nursing Diagnosis Impaired verbal communication related to brain injury Nursing Interventions Assess comprehension Stand on patients unaffected side (stay within patients visual field) Keep environment simple and relaxed; minimize distractions Speak at normal rate and volume since patient is not hard of hearing ,and there is no intellectual impairment Allow plenty of time to answer Dont ask questions requiring complex answers Provide pad and pens if patient prefers and is able to write Avoid forcing speech Watch for clues and gestures if speech is jargon
ANEURYSMAL SUBARACHNOID HEMORRHAGE
Aneurysm is an abnormal localized dilatation of a blood vessel from congenital defect or absence of the muscle layer of the vessel
Most
are asymptomatic until rupture and produce symptoms of hemorrhagic stroke
Aneurysmal subarachnoid hemorrhage represents bleeding into the subarachnoid space caused by a ruptured cerebral aneurysm A dreaded complication of cerebral aneurysm
ARTERIOVENOUS MALFORMATION
Complex tangle of abnormal arteries and veins linked by one or more fistulas A system of dilated rteies and veins in which the normal capillary bed is absent A tangle mass of discolored vessels that have the appearance of a cluster of grapes Approximately 50% of patients with AVM presents with hemorrhage
ARTERIOVENOUS MALFORMATION Hemodynamic effects

Blood
passes from the high pressure arteries to the low pressure veins without passing through the capillaries due to their absence The draining venous channels are exposed to high levels of pressure predisposing them to rupture and hemorrhage Impaired perfusion affects cerebral tissues adjacent to the AVM leading to slowly progressive neurologic deficits referred to as Vascular Steal Phenomenon
ARTERIOVENOUS MALFORMATION

AVM is typically present before 40 years of age Affects men and women equally Accounts for approximately 2% of strokes
Manifestations include hemorrhage, seizures, headaches, progressive neurologic deficits 50% present with intracerebral hemorrhage SAH and intraventricular hemorrhage also occur Headache: severe, throbbing and synchronous with their heartbeat Diplopia, hemianopia, hemiparesis, mental deterioration and speech deficits
Manifestations
Sudden,
severe headache, described as the worst headache of my life accompanied by nausea, vomiting and dizziness Signs of meningeal irritation such as nuchal rigidiy (neck stiffness), photophobia (light intolerance), cranial nerve deficits esp. CNs II, III, and IV (diplopia and blurred vision), storke syndrome, loss of consciousness, increased ICP, pituitary dysfunction
ANEURYSMAL SUBARACHNOID HEMORRHAGE AND ARTERIOVENOUS MALFORMATIONS
Clinical
presentations CT scan- most commonly used method to detect SAH Lumbar puncture- to detect blood in CSF Cerebral Angiography definitive diagnostic tool to detect aneurysm and AVM; also detect vasospasm
Complications
Rebleeding,
vasospasm,
with cerebral ischemia, hydrocephalus, hypothalamic dysfunction, and seizure activity
DEMENTIAS
Syndrome of intellectual impairment or deterioration severe enough to interfere with occupational or social performance May involve disturbances in memory, language use , perception, and motor skills May interrupt ability to learn necessary skill, solve problems, think abstractly and make judgment Sometimes called Senility is not a normal aging process A major cause of disability in the older population
DEMENTIAS
2.5% to 24.6% of those older than 65 years of age In long-term care facilities, up to 70% of residents have cognitive impairments Causes: disorders such as:
Degenerative Vascular Neoplastic Demyelinating Infectious Inflammatory Toxic Metabolic psychiatric
DEMENTIAS
Types of Dementia Alzheimers disease most common Vascular/multi-infarct dementia 2nd most common Picks disease Creutzfeldt-Jakob disease Wernick-Korsakoff Syndrome Huntingtons disease
OTHER TYPES OF DEMENTIA

Vascular Dementia/multi-infarct dementia associated with cerebrovascular disease from multiple infarctions through out the brain 2nd most common, 20% to 25% of dementias Incidence closely associated with hypertension Other contributing factors: arrhythmias, MI, peripheral vascular disease, DM, and smoking Gradual or abrupt onset Focal neurologic symptoms related to local areas of infarction

Picks disease

Rare form of dementia characterized y atrophy of frontal and temporal areas of brain Neurons contain cytoplasmic inclusions known as Pick bodies Average onset: 38 years More common in women and men Behavioral manifestation such absence of concern and care, loss of initiative, repetition, hypotonia, incontinence, noticed earlier than memory loss Short course, death within 2 to 10 years from infection

Creutzfeldt-Jakob disease

Rare transmisible form of dementia Caused by an infective protein called prion : lack a genome, a mutated protein, that when accumulates in high concentration in neurons lead to a toxic condition and cell death Transmitted through corneal transplant and human growth hormone taken from cadavers Causes degeneration of pyramidal and extrapyramidal systems Has a rapid course; demented at 6 month of onset Fatal, death within months; few may survive for several years Symptoms include personality changes, dementia, insomnia and ataxia as disease progresses

Wernicke-Korsakoff syndrome

Result from chronic alcoholism Wernickes disease is characterized by acute weakness and paralysis of extraocular muscles, nystagmus, ataxia, and confusion as well as peripheral neuropathy Signs from alcohol withdrawal: delirium, confusion, hallucination Cause: deficiency of thiamine (vit. B 1) Symptoms are reversed when nutrition is improved with supplemental thiamine
Wernicke-Korsakoff syndrome
Korsakoff
syndrome
Chronic phase with severe impairment of recent memory Characterized by difficulty in dealing with abstractions and defective capacity to learn Confabulations (recitation of imaginary experiences to fill gaps in memory) most distinctive feature of the disease Polyneuritis is common Does not improve significantly with treatment

Huntingtons Disease

Also known as Huntingtons chorea Rare hereditary degenerative d/o characterized by chronic progressive chore, psychological changes, and dementia An autosomal dominant disorder: gene in chromosome 4 Age of onset: 4th and 5th decades By the time diagnosis is made, gene has already been passed on to the children Occurs in 5 per 100,000 persons
HUNTINGTONS DISEASE
Pathophysiology
Principal pathologic feature:
Severe degeneration of the basal ganglia particularly the caudate and putamine nuclei and frontal cortex causing a decrease in GABA synthesis and secretion resulting decrease inhibitory activity on the dopaminergic pathway and decrease in acetylcholine level leading to increase dopaminergic activity in the basal ganglia with the cerebral cortex leading to hypotonia and hyperkinesia (involuntary, fragmentary movement such as chorea)
HUNTINGTONS DISEASE
Clinical Manifestations Abnormal movement and progressive dysfunction of intellectual processes (dementia) and thought processes Chorea (to dance) or choreiform movement (sudden jerky and irregular but coordinated, and graceful movement beginning in face, and arms, and eventually affecting the entire body Impaired memory and judgment, impulsive behaviors Delusions and depressions
HUNTINGTONS DISEASE
Based on family history and clinical presentations Genetic testing: disease marker G8 on chromosome 4
HUNTINGTONS DISEASE
Management
No cure for the disease Treatment: symptomatic Drugs used to treat dyskinesias and behavioral disturbances
Progressive degenerative d/o of the cerebral cortex Senile Dementia Dementia impairment of intellectual function, usually accompanied by memory loss and personality changes Profound loss of memory, cognition and ability for self-care Poor prognosis 2 15 years (death) ; average of 8 years unknown etiology Contributing factors: Neurotransmitter deficiency (acetylcholine & norepinephrine) Viral factors Trauma Genetic factors : 70% - chromosome abnormality at C21 Positive protein: Amyloid plaques damages brain tissue (death of neurons) Commonly affects frontal, pareital and occipital lobes
Clinical manifestations
1.

Stage 1
Lasts 2 - 4 years Memory loss (recent memory) Difficulty with abstract thinking & mathematical tasks Lack of spontaneity Loss of sense of humor Disorientation to the time and date Lack of energy
2.

Stage 2
Lasts several years Impaired cognition and abstract thinking Restlessness and agitation Wandering ---> Sundowning (wandering in the late afternoon and evening) Inability to carry out ADL Impaired judgment & impulse control Inappropriate social behavior
Clinical manifestations
3. Stage 3 Usually lasts only for 1-2 years but can last as long as 10 years Emanciation Indifference to food Inability to concentrate Urinary and fecal incontinence Seizures
Interventions :
Institute safety measures Side rails up & bed in low position Check patient frequently, especially at night Use restraints only when absolutely necessary and with a doctors order Never leave anything at the bedside that could harm the patient Approach the client with a friendly, relaxed manner patients mirror the affect of those around them Orient client to person, time and place frequently Label items, use visual cues like pictures For hyperactive clients: finger-foods Schedule activities & tests in the morning & early afternoon to avoid overstimulation at bedtime Cholinesterase inhibitors : for cognitive impairment
donepezil (Aricept) taccrine (Cognex) rivostigmine (Exxelon)
The Five (5) Cs of Alzheimers Management:

1. 2. 3. 4. 5. Use of Calendar Use of Clock Use of Colors Consistency of Caregiver Administration of Cognex (tacrine) to increase mental ability
degenerative disease resulting in dysfunction of the extrapyramidal system responsible for voluntary movement Deficiency of Dopamine in the Substantia nigra Vs. Acetylcholine 50 60 years of age Cause: unknown Factors: Genetics Atherosclerosis viral infection head trauma Cerebrovascular Accident CO destroys cells of the substantia nigra in the basal ganglia
Assessment :
Cardinal Signs: Resting tremors pill-rolling tremors (initial manifestation) Increases when stressed, anxious or concentrating Decreases with purposeful activity and sleep Muscle rigidity (Cogwheel rigidity) - movements are jerky and stiff Bradykinesia abnormally slow movements Difficulty initiating movement Freezing phenomenon (extreme form) Propulsive, shuffling gait and decrease in arm swing Stooped posture, microphonia Difficulty rising from sitting position Mask-like face with decreased blinking of the eyes Fatigue, emotional lability Muscle weakness - affected eating - chewing - swallowing - speaking Autonomic disorder - salivation, sweating, orthostatic hypotension
Management:
Medications Levodopa (L- dopa / Larodopa / Dopar) Converted to dopamine in the body Increases dopamine levels Relieves tremors, rigidity & bradykinesia Give with meals to decrease GI distress Avoid coffee can increase Nausea Postural hypotension Carbidopa Levodopa (Sinemet) Prevents breakdown of dopamine Fewer side effects Amantadine (Symmetrel) For mild cases Decreases rigidity, tremor & bradykinesia
Management:
Anticholinergics - Trihexyphenidyl (Artane), Benztropine (Cogentin), Biperiden (Akineton) Inhibit action of acetylcholine For mild cases / relieves tremors and rigidity Antihistamines decreases tremors and rigidity Antispasmodics improves rigidity Deprenyl prolong the action of levodopa Bromocriptine (Parlodel) / Pergolide stimulates dopamine release Used when levodopa loses its effectiveness
Management:
Provide safe environment side rails on bed, handlebars on toilet, bathtub and hallways, remove hazards that might cause falls, use rubber soled shoes & low heels Maintain adequate nutrition, allow sufficient time for meals Remember in teaching the client: intellect is usually not impaired High fiber and fluids to prevent constipation from the anti-cholinergic drugs Low-protein diet at daytime because it decreases absorption of Levodopa which is usually given at daytime High-protein diet at night
Chronic, progressive, non-contagious degenerative disease of the CNS characterized by demyelination of the neurons Demyelination destruction of myelin sheath of the nerve fiber in the brain & spinal cord Most disabling neurologic disease in young adults during their productive years, characterized by remissions & exacerbations Frequently involves the optic, oculomotor & spinal nerve tracts Affects women more than men, 20 40 years old Etiology: unknown Theories: infection, autoimmune response, allergic reaction, trauma, anoxia, toxins, stress, fatigue & vascular lesions destroy axons and myelin sheath
Damaged myelin sheath impairs the normal conduction of the nerves Usually affects : Optic nerves & Oculomotor nerves: visual problems Cerebellum : timing, coordination of skeletal muscle activity and balance Brainstem Midbrain Vision & hearing (corpora quadrigemina) Pons control of breathing Medulla Oblongata HR, BP, vomiting, swallowing & breathing
Assessment: Charcots Triad : nystagmus, intention tremor & speech deficits Ataxia, loss of coordination Diplopia initial manifestation Fatigue, weakness, numbness, tingling, loss of position sense & paralysis Bladder & bowel incontinence Dysphagia Emotional instability, mood swings & impaired judgment Pain due to muscular spasm Blurred vision, scotomas (blind spots) Sexual impotence in males Impaired sensation: touch, pain, cold & warmth CSF contains abnormal amounts of IgG antibodies MRI shows areas of demyelination
Management: Avoid precipitation of exacerbations Avoid fatigue, stress, infection, extremes in temperature Establish regular program of exercise & rest Balanced diet Medications Acute Exacerbations: Corticosteroids to decrease edema at sites of demylination For spasticity lioresal (Baclofen), dantrolene (Dantrium) or diazepam (Valium) To alter immune response Interferon (still experimental) Mood swings chlordiazepoxide (Librium) Encourage self-care activities Prevent complications of immobility DVT, bed sores & contractures Promote safety & prevent injury
Disorder affecting the NM transmission of voluntary muscles Produces sporadic, progressive weakness & abnormal fatigue of voluntary muscles exacerbated by exercise & repeated movements and is relieved by rest Patient gets tired on exertion even by just combing hair, chewing or talking Common in women: 15-35, men: above 40 Pathology:
Autoimmune: antibodies attach to Ach receptor sites blocking, destroying & weakening them, leaving them insensitive to acetylcholine Deficiency in Acetylcholine Excess Acetylcholinesterase
usually affects muscles innervated by the cranial nerves : face, lips, tongue, neck, throat, eyes, head control, chewing, swallowing, speech, etc. When it involves the muscles for breathing life-threatening!
Assessment: Diplopia (double vision) Ptosis Sleepy, mask-like expression Droopy jaw Extreme muscle weakness (initial manifestation) Fatigue Weak voice Difficulty in chewing, swallowing, closing of mouth or smiling Weakness of arm, hand & leg muscles Progressive weakness of diaphragm & intercostal muscles difficult breathing Bobbing head
DIAGNOSTIC EVALUATIONS

Serum test for Ach receptor antibodies Edrophonium (Tensilon) test IV Provides spontaneous relief of symptoms (lasts 5-10 minutes) CT Scan of the neck area thymoma & thymus hyperplasia Electrophysiologic testing decremental response to repetitive nerve stimulation
Management: Medications Steroids Anticholinesterase Drugs Increases acetylcholine levels at the NM junction Pyridostigmine bromide (Mestinon) Neostigmine bromide (Prostigmine) Nsg resp: Give meds exactly on time Give 30 minutes before meals Give with milk and crackers to avoid GI upset Monitor effectiveness : assess muscle strength Avoid drugs that block NM transmission Morphine SO4 Strong sedatives ether, novocaine, curare Streptomycin, kanamycin, neomycin & gentamycin
Management:

Plasmapheresis (plasma exchange) Thymectomy Promote optimal activity Short periods of activity, long periods of rest Time activity with max muscle strength Encourage normal ADL Promote optimal nutrition Mealtime coincide with peak effect of drug Check gag reflex & swallowing ability before feeding Promote mechanical soft diet
Myasthenic Crisis: Abrupt onset of severe, generalized muscle weakness Sudden respiratory distress failure Cause: Undermedication Stress Infection or trauma Symptoms improve with Tensilon Test Care: Maintain tracheostomy or E-tube to assist with ventilation ABGs Bedrest Increase Anticholinesterase drugs
Cholinergic Crisis: Abrupt onset of severe, generalized muscle weakness Sudden respiratory distress failure S/E of Anticholinesterse drugs
Abdominal cramps, diarrhea, N&V, excessive salivation, excessive sweating
Cause: Overmedication of Anticholinesterase drugs Symptoms worsen with Tensilon Test Care: Maintain tracheostomy or E-tube to assist with ventilation ABGs Bedrest Discontinue Anticholinesterase drugs Give Atrophine SO4
Polyradiculoneuritis Rapidly progressing syndrome of unknown cause involving the peripheral sensory and motor nerves and nerve roots Segmented demyelination of the peripheral nerves Age: 30 50 years old Characterized by ascending paralysis Theories: Autoimmune disorder Predisposing factors: Recent viral infection Recent immunization 30 40% follows a Campylobacter infection (infectious diarrhea)
Assessment: Clumsiness usually the first sign Paresthesia (tingling/numbness) often starting at the legs, ascending to the upper extremities, trunk and face Paralysis of facial, ocular and oropharyngeal muscles Difficulty in swallowing, chewing and talking Progressive, ascending motor paralysis Ventilatory insufficiency if paralysis ascends to the respiratory muscles Considered a medical emergency May require mechanical ventilation
Management:
Maintain adequate ventilation

Monitor RR, maintain open airway, suction secretions Assist with Endotracheal intubation and mechanical ventilation as indicated
V/S Corticosteroids to suppress immune response Prevent complications of immobility Promote comfort Optimum nutrition

Gag reflex Pureed foods Assess need for NGT
Rehab training to regain strength refer to PT Plasmapheresis
AMYOTROPHIC LATERAL SCLEROSIS

Also known as Lou Gehrigs disease after the famous New York Yankee baseball player Incapacitating/devastating neurologic disease resulting in progressive weakness accompanied by other lower motor neuron signs such as atrophy or fasciculation Affects upper and lower motor neurons Amyotrophic means without muscle nutrition or progressive muscle wasting refers to the LMN component of the syndrome Lateral sclerosis scarring of the corticospinal tract in lateral column of spinal cord refers to the UMN component of the syndrome

A disorder of middle to late adulthood May begin anytime in the 4th decade of life Peak of occurrence is in the early 50s Male to female ratio: 3 or 3 is to 1 Follows a progressive course with mean survival period of 2 to 5 years from onset of symptoms

Cause is unknown 5% to 10% of cases are familial Mutation of gene encoding superoxide desmutase 1 (SOD1) was mapped to chromosome 21. SOD1 functions in the prevention of free radical formation Mutation accounts for 20% of familial ALS Remaining 80% caused by mutations in other genes Exotoxic injury from glutamate excitotoxicity = increased glutamine in CSF of patients with ALS
Other possible cause under investigation:

Viral-immune
factors
Metabolic Nutritional
Systemic
stimuli such infection or
trauma Serum immune complexes are elevated in ALS but nature of complexes is unknown
Pathophysiology
Degeneration
of upper motor neurons (nerve leading from the brain to the medulla or spinal cord) and lower motor neurons (nerves leading from spinal cord to the muscles of the body) progressive loss of voluntary, muscle contraction and functional capacity Death of neurons result in axonal degeneration and secondary demyelination with glial proliferation and sclerosing (scarring)

Clinical Manifestations
UMN lesion
Weakness,
and spasticity or stiffness Impaired fine motor control Dysphagia (difficulty swallowing) Dysarthria (impaired articulation of speech0 Dysphonia (difficulty making the sounds of speech)
LMN lesion
progressive
with wasting of muscles of arms, trunk and legs, fasciculation, hyporeflexia, loss of body hair, decreased sweating Muscle cramp involving the distal legs is an early symptom
Progressive weakness and atrophy of distal muscles of one upper extremity followed by regional spread of clinical weakness (reflects involvement of neighboring areas of spinal cord leading to involvement of UMN and LMN in limbs and head affecting muscles of palate, pharynx, tongue, neck, and shoulders causing impairment of swallowing, chewing, and speech. Dysphagia with recurrent aspiration and weakness of respiratory muscles Death results from involvement of cranial and respiratory muscles
Course of the Disease
Average duration of life is approximately 2 to 3 years from appearance of symptoms May run from a few months to 15 years 20% survive 5 to 20 years


Electromyography evaluates denervation and muscle atrophy Nerve conduction study evaluates nerve pathways Barium swallow - evaluates ability to achieve various phases of swallow MRI, CT rule out other disorders Lab tests rule out other causes of muscle weakness

Management
Currently, there is no cure/ no specific treatment to arrest or alter disease progression. Treatment is palliative and symptomatic Rehabilitation measures assist persons to manage disability together respiratory and nutritional support to survive longer Riluzole antiglutamate drug, to decrease accumulation of glutamate and slow the progression of the disease. Drug prolonged survival by 3 to 6 months

Symptomatic treatment: Baclofen to control spasticity Diazepam to control fasciculations Antidepressants, sleep medications Feeding gastrostomy Mechanical ventilation, eventually becomes necessary
Complications
Respiratory failure Aspiration pneumonia
Respiratory arrest
AMYOTROPHIC LATERAL SCLEROSIS Nursing Assessment

Based on History and PE
Respiratory status and function

Cranial nerve functions; gag reflex and wallowing Voluntary motor function and strength

Nursing Diagnoses
Ineffective breathing pattern related to respiratory muscle weakness Impaired physical mobility related to disease process Altered nutrition: LBR related to inability to swallow Fatigue related to denervation of muscles Social isolation related to fatigability and decreased communication skills Risk for infection related to inability to clear airway

Nursing Interventions Goals Maintain respiration Optimize mobility Meet nutritional requirements: high calorie, small frequent feedings, semisolid Minimize fatigue Maintain social interaction Prevent aspiration and infection

Outcome-based Evaluation Respirations unlabored Feeding self with assistive utensils, w/o aspiration Napping twice a day, Communicating needs effectively to staff and family No signs of respiratory or urinary infections
CNS INFECTIONS
Meningitis - inflammation of the meninges of the brain and spinal
cord, caused by bacteria, viruses, or other microorganisms. Encephalitis - inflammation of the brain, caused by a virus; may occur as a sequela of measles, mumps, chickenpox. Signs and symptoms: headache (initial manifestation), photophobia, irritability, chills, fever, vomiting possible seizures,decreasing LOC signs of meningeal irritation - nuchal rigidity: stiff neck - opisthotonos: head and heels bent backward and body arched forward - Kernigs sign - Brudzinkis sign Tests: Lumbar puncture- measurement and analysis of CSF shows increased pressure, elevated WBC and protein, decrease glucose and culture positive for specific microorganism.
KERNIGS SIGN Present if lower leg cannot extend due to pain and spasm when client is lying supine with one leg bent over his abdomen.
BRUDZINSKIS SIGN Present if the clients hips and knees flex when he is lying supine with his head lifted towards his chest.
Management:
give large doses of antibiotics as ordered dexamethasone digoxin to help control arrythmias mannitol to decrease cerebral edema enforce respiratory isolation after initiation antibiotic therapy for some types of meningitis give nsg. care for increased ICP, seizures, and hyperthermia provide nsg. Care for delirious or unconscious client as needed bed rest keep room quiet & dark if photophobia or headache occurs maintain fluid and electrolyte balance prevent complications of immobility monitor vital signs and neuro checks frequently teach client concerning discharge plans: - maintain a good diet high in protein, high calories, with small frequent feedings - rehabilitation program for residual deficits refer patient to Audiologist, hearing impairment is a common complication of meningitis
episodes of abnormal motor, sensory or autonomic due to

abnormal discharge from brain cells. Epilepsy - chronic recurrent seizures. may be caused by : infantile fever head injury hypertension CNS infection brain tumor or metastasis drug withdrawal (alcohol / barbiturates) stroke trauma subdural hematomas circulatory disorders drug toxicity: lidocaine, penicillin, theophylline unknown
TYPES:
Generalized seizures Major motor seizure (grand mal) aura, usually starts with tonic or stiffening phase, followed by clonic or jerking phase; may have bowel/ bladder incontinence; then in postictal phase, sleeps / loss of consciousness, lasts 2-5 minutes Absence seizure(petit mal) sudden onset, with twitching or rolling of eyes; lasts a few seconds, appears daydreaming Febrile seizures - common under 5yrs. of age; seizure occurs only when fever is rising; EEG is normal 2 weeks after a seizure Atonic or akinetic seizure drop seizure sudden, momentary loss of muscle tone, usually falls to the ground
Partial seizures
Simple partial seizure - seizure confined to one hemisphere of the brain, no LOC; may report de ja vu Complex partial seizure - begins in focal area but spreads to both hemispheres; impairs consciousness; maybe preceded by an aura - mannerisms : (client is unaware) lip smacking, chewing, picking at clothes, jerking movements Jacksonian seizure - twitching begins at distal end of extremity, eventually involving entire extremity and possibly entire side of the body; no LOC; not commonly seen in children
Status epilepticus
- usually refers to grand mal seizures; prolonged ( repeated seizures without regaining consciousness) and unresponsive to treatment; can result in hypoxia and possible cardiac arrest
MANAGEMENT
During seizure activity protect from injury: prevent falls support head decrease external stimuli do not restrain dont use tongue blades or insert anything in the mouth keep airway open: side lying position, suction excess mucous, loosen clothing observe and record seizure - note any preictal aura: fear, anxiety, hallucinations, dj vu symptoms - note nature of the ictal phase: symmetry of movement, response to stimuli, LOC, respiratory pattern - note postictal response: amount of time it takes to orient to time and place; sleepiness Provide client teaching and discharge planning need to drug therapy wear a Medic-Alert identification bracelet or carry ID availability of support groups and community agencies
Drug therapy : (Anticonvulsants)

Phenytoin (Dilantin) most commonly used can only be administered with in normal saline and levels are monitored to titrate dosage therapeutic level is 10-20 mg/dl side effects include gum hyperplasia, hirsutism, ataxia, gastric distress, nystagmus, anemia, sedation Diazepam (Valium) drug of choice for status epilepticus monitor RR Valproic Acid (Depakene) used to treat absence seizures Phenobarbital Na used for general and absence seizures Tegretol (Carbamazepine) used when seizure have not responded to other anticonvulsants give with meals
Surgery to remove the tumor, hematoma or epileptic focus
GINGIVAL HYPERPLASIA
Localized intracranial neoplasm that occupies space & cause a rise in intracranial pressure Benign or malignant 2nd most common cancer in children Supratentorial location adults Infratentorial location children
Tumor
from the meninges Meningioma Tumors in the cranial nerves Acoustic neuroma Optic nerve spongioblastoma Metastatic cancers lung carcinoma breast cancer Blood vessel tumor hemangioblastoma angioma
Symptom due to increase ICP Changes in behavior Restless, drowsiness Pupillodilation Headache in the morning Projectile vomiting VS : increase BP, bradycardia and irregular respiration Localized neurologic impairement Motor weakness, paralysis, lack of coordination, ataxia, dysphagia Sensory vision disturbances, problems of hearing, no touch, pressure, position sense
Management :
Dexamethasone Anticonvulsants Antacids & H2antagonist Radiation therapy Surgery Chemotherapy
HEAD INJURY
usually caused by car accidents, falls, assaults
Types: Concussion Contusion Hemorrhage
CONCUSSION
severe blow to the head jostles brain causing it to strike the skull; results in temporary neural dysfunction
CONTUSION
results from more severe blow that bruises the brain and disrupts neural function
HEMORRHAGE
epidural hematoma accumulation of blood between the dura mater and skull; commonly results from laceration of middle meningeal artery during skull fracture; blood accumulates rapidly subdural hematoma accumulation of blood between the dura and arachnoid; venous bleeding that forms slowly; may be acute, subacute, or chronic
HEMORRHAGE
subarachnoid hematoma bleeding in the subarachnoid space intracerebral hematoma accumulation of blood within the cerebrum
ASSESSMENT FINDINGS
Concussion headache, transient loss of consciousness, retrograde or posttraumatic amnesia, nausea, dizziness, irritability Contusion neurologic deficits depend on the site and extent of damage; include decreased LOC, aphasia, hemiplagia, sensory deficits
ASSESSMENT FINDINGS
Hemorrhages a. epidural hematoma - brief loss of consciousness followed by lucid interval; progresses to severe headache, vomiting, rapidly deteriorating LOC, possible seizure, ipsilateral papillary dilation
ASSESSMENT FINDINGS
b. subdural hematoma - alterations in LOC, headache, focal neurologic deficits, personality changes, ipsilateral papillary dilation c. intracerbral hematoma - headache, decreased LOC, hemiplegia, ipsilateral papillary dilation
NURSING INTERVENTIONS
Maintain a patent airway an adequate ventilation Observe for CSF leakage a. bloody spot encircled by watery, pale ring on pillowcase or sheet b. never attempt to clean the ears or nose of a head-injured client or use nasal suction unless cleared by physician
NURSING INTERVENTIONS
4. If a CSF leak is present a. instruct client not to blow nose b. elevate head of bed 30 degrees as ordered d. place a cottonball in the ear to absorb otorrhea; replace frequently
SPINAL CORD INJURIES

- occurs most commonly in young adults male between ages 15 and 25 -causes motor vehicle accidents, diving in shallow water, falls, industrial accidents, sports injuries, gunshot or stab wounds - nontraumatic causes tumors, hematomas, aneurysms, congenital defects (spina bifida)
PATHOPHYSIOLOGY
Hemorrhage and edema cause ischemia, leading to necrosis and destruction of the cord
MEDICAL MANAGEMENT
1. Horizontal turning frames 2. Skeletal traction: a. Cervical tongs inserted through burr holes; traction is provided by a rope extended from the center of tongs over a pulley with weights attached at the end
CERVICAL TONGS
MEDICAL MANAGEMENT
b. Halo traction 1) stainless steel halo ring fits around the head and is attached to the skull with four pins; halo is attached to plastic body cast or plastic vest
2) permits early mobilization, decreased period of hospitalization and reduces complications of immobility
ASSESSMENT FINDINGS
1. Spinal shock - characterized by absence of reflexes below the level of the lesion, flaccid paralysis, lack of temperature control in affected parts, hypotension with bradycardia, retention of urine and feces quadriplegia cervical injuries (C1-C8) cause paralysis of all four extremities; respiratory paralysis occurs in lesions above C4 due to lack of innervation to the diaphragm paraplegia thoraco/lumbar injuries (T1-L4) cause paralysis of the lower half of the body involving both legs
ASSESSMENT FINDINGS
1) complete cord transaction a) loss of all voluntary movement and sensation below the level of the injury; reflex activity below the level of the lesion may return after spinal shock resolves b) lesions in the conus medullaris or cauda equine result in permanent flaccid paralysis and areflexia 2) incomplete lesions varying degrees of motor or sensory loss below the level of the lesion depending on which neurologic tracts are damaged and which are spared
NURSING INTERVENTIONS: EMERGENCY CARE

1. assess airway, breathing, circulation a. do not move the client during assessment b. if airway obstruction or inadequate ventilation exists: do not hyperextend neck to open airway, use jaw thrust instead 2. perform a quick head-to-toe assessment: check for LOC, signs of trauma to the head or neck, leakage of clear liquid from ears or nose, signs of motor or sensory impairment 3. immobilize the client in the position found until help arrives
NURSING INTERVENTIONS : ACUTE CARE

Maintain optimum respiratory function Maintain optimal cardiovascular function change position slowly and gradually elevate the had of bed to prevent postural hypotension . Maintain immobilization and spinal alignment always a. turn every hour on turning frame b. maintain cervical traction at all times if indicated
Maintain urinary elimination maintain bowel elimination: administer stool softeners and suppositories to prevent impaction as ordered Monitor temperature control
Observe for and prevent infection

10. Observe for and prevent stress ulcers a. assess for epigastric or shoulder pain b. if corticosteroids are ordered, give with food or antacids; administer cimetadine (Tagamet) as ordered c. Check nasogastric tube contents and stools for blood
NURSING INTERVENTIONS CHRONIC CARE

1. Neurogenic bladder reflex or upper motor neuron bladder; reflex activity of the bladder may occur after spinal shock resolves; the bladder is unable to store urine very long and empties involuntarily
nonreflexive or lower motor neuron bladder: reflex arc is disrupted and no reflex activity of the bladder occurs, resulting in urine retention with overflow

c. management of reflexive bladder intermittent catheterization every 4 hours and gradually progress to every 6 hours
regulate fluid intake to 1800- 2000 cc/day

bladder taps or stimulating trigger points to cause reflex emptying of the bladder

d. Management of nonreflexive bladder intermittent catheterization every 6 hours
Crede maneuver or rectal stretch regulate intake to 1800- 2000 cc/day to prevent overdistention of bladder

2. Spasticity drug therapy : baclofen (Lioresal), dantrolene (Dantrium), diazepam (Valium)
physical therapy stretching exercises, warm tub baths, whirlpool surgery chordotomy
A birth defect where the backbone and spinal canal do not close before birth, which allows the spinal cord and the covering membranes to protrude out of the child's back. causes: genetic, viral, radiation, intrauterine folic acid deficiency Types * spina bifida occulta * spina bifida cystica - meningocele - meningomyelocele/ myelomeningocele (75% of cases) Symptoms - visible sac-like protrusion on the mid to lower back-not translucent when a light is shone from behind the sac Meningomyelocele: motor and sensory deficit below the lesion Spina bifida occulta may be indicated by: - a tuft of hair at the sacral area (back part of the pelvis) dimpling of the sacrum
MANAGEMENT
prevent trauma to the sac - cover with sterile dressing soaked with normal saline - position prone or side lying - keep area free from contamination by urine or feces - inspect for signs of infection provide adequate nutrition, high fiber diet provide sensory stimulation prevent complications aid the family in coping with the disorder surgery is usually done within 48 hours after birth to lower the risk of infection, swelling, and further damage.
AUTONOMIC DYSREFLEXIA
rise in blood pressure, sometimes to fatal levels occurs in clients with cord lesions above T6 and most commonly in clients with cervical injuries stimulus may be overdistended bladder or bowel, decubitus ulcer, chilling, pressure from bedclothes
SYMPTOMS
severe headache hypertension bradycardia, sweating goosebumps nasal congestion blurred vision convulsion
INTERVENTIONS
raise client to sitting position to decrease BP check for source of stimulus (bladder, bowel, skin) remove offending stimulus (catheterize client, digitally remove impacted feces, reposition client monitor blood pressure
INTRACRANIAL SURGERY
1.
Craniotiomy surgical opening of skull to gain access to intracranial structures; used to remove a tumor, evacuate blood clot, control hemorrhage, relieve increased ICP
2. Craniectomy excision of a portion of the skull; sometimes used for decompression 3. Cranioplasty repair of a cranial defect with a metal or plastic plate
BRAIN AND SPINAL ABSCESS

Localized collections of pus within the parenchyma of the brain and spinal cord Between the dura and arachnoid linings (subdural empyema) Between the dura and skull (cranial epidural abscess) Spinal cord abscesses occur in epidural, subdural, intermedullary regions
Incidence is 1 in every 100, 000 hospital admissions
Male to female ratio: 2 is to 1

Median age is 30 to 40 years of age

Brain abscess- results from direct inoculation of organisms from paranasal sinuses, middle ear, teeth, penetrating injury, cranial surgery or bacteremias from extrcranial sources: heart, lungs, pelvic organs, kin, tonsils Sinusitis: primary source of infection in as many as 2/3 of intrcranial abscesses
Etiologic agents:
aureus etiologic agent in 60% of spinal epidural abscesses Staphylococci Bacteroids Toxoplasma gondii in persons with AIDS Fungal brain abscess: in persons with HIV and immuno-compromised persons: Candida species M. tuberculosis
S.

Intramedullary abscesses are more common in pediatric population 8% are located in cerebrum 20%: cerebellum Most common sites: frontal and temporal lobes 5% to 20% of cases occur in more than one site
Classifications (Brain Abscess)

associated with osteomyelitis in a cranial bone Intracerebral arise from vascular source
Extradural
Classifications (Spinal cord abscess)

epidural abscess form in epidural space, those with diabetes mellitus show increased incidence, originate as osteomyelitis in a vertebra Intramedullary spinal cord abscess form within spinal cord, those with sepsis
Spinal

Pathophysiology Organisms gain entrance to CNS via direct extension of osteomyelitis or via a vein localized inflammation (focal cerebritis) edema, hyperemia, softening, petechial hemorrhage exudate formation, septic thrombosis of vessels, and aggregates of leukocytes and fibrin encapsulation of purulent focus by fibroblasts from capillaries adjacent to the focal cerebritis limiting its spread Encapsulation takes about 2 to 3 weeks Free non-encapsulated abscess: associated with higher mortality
Abscess is composed of 3 layers:

A
center of polymorphonuclear leukocytes A collagenous capsule Peripheral gliosis
Existing abscess tend to spread and form daughter cells

Clinical Manifestations Abscesses are associated with: Intracranial infection:
fever
(in less than 50% of cases, increased sedimentation rate (poorly localized with a dull ache) most frequent early symptom, increased ICP such as nausea, vomiting, decreased LOC, decreasing cognitive abilities, paresis, seizures
Expanding intracranial mass:

headache

Clinical Manifestations Early manifestations: Low-grade fever Headache Neck pain and stiffness with mild nuchal rigidity Confusion Drowsiness Sensory deficits Communication deficits

Clinical Manifestations Later manifestations: Inattentiveness (distractibility) Memory deficits Decreased visual acuity Narrowed visual fields Papilledema Ocular palsy Ataxia Dementia
Extradural abscess
Associated
with:
localized pain, purulent drainage from nasal passages or auditory canal, fever, localized tenderness, neck stiffness, focal seizure

Clinical Manifestations (Spinal cord abscess) Four stages:
Spinal Root
aching
pain: usually severe, with spasm of back muscles and limited vertebral movement in 94% of patients
Weakness
Paralysis
from progressive cord compression

Suggested on the basis of clinical features and confirmed by: CT Scan, MRI: to locate site of abscess and differentiate it from metastatic tumor Blood cultures: to identify organism, (+) gram stain, leukocytosis, elevated ESR Cultures from suspected source of infection EEG for seizures
Management

Closed stereotaxic needle biopsy under Ct guidance for drainage evacuation instead of craniotomy Radical surgical debridement Antimicrobial therapy- for 6-8 weeks parenterally followed by a 2-3 month course of oral therapy Antifungal therapy (Amphotericin B) for candidiasis and other fungal infections Antitubercular therapy for AFB Corticosteroid and osmotic diuretics to reduce cerebral edema Anticonvulsants for seizures

Complications Rupture into the ventricular space leading to sudden increase in severity of headache, fatal Papilledema in 25% of cases indicating intracranial hypertension Lumbar puncture is dangerous: may lead to brain stem herniation Permanent neurologic deficits: seizure disorders, visual defects, hemiparesis, CN palsies Greater mortality for symptoms with short duration, severe mental changes, and rapid progression of neurologic impairment

Nursing Assessment History of previous infection, immunosuppression, headache, and related symptoms Neurologic assessment: CN, motor, and sensory status evaluation
BRAIN AND SPINAL ABSCESS Nursing Diagnoses
Pain
Altered thought process Risk for injury Anxiety

Nursing Interventions
Relieve pain: analgesics as ordered, comfort measures, proper head position, relaxation techniques Promote thought processes: frequent monitoring of v/s, LOC, orientation, and seizures Minimize neurologic deficits: protect from injury, refer to occupational, speech therapies, and rehabilitation Reduce anxiety: inform about disease process, procedures, etc.

Evaluation Verbalized reduced pain Patient oriented to time, place, and person, follows simple commands No injury related to neurologic deficits Reduced anxiety
ANTIMYASTHENIC MEDICATIONS
Relieve muscle weakness associated with myasthenia gravis by blocking acetylcholine breakdown at the neuromuscular junction
Used to treat or diagnose myasthenia gravis or to distinguish cholinergic crisis
ANTIMYASTHENIC MEDICATIONS
Edrophonium chloride (Tensilon, Enlon) Neostigmine bromide (Prostigmin Bromide)
SIDE EFFECTS: CHOLINERGIC CRISIS
GI disturbances Abdominal cramps Nausea, vomiting, diarrhea Increased salivation and tearing Increased bronchial secretions Sweating Miosis Hypertension
IMPLEMENTATION
Monitor the client for signs and symptoms of medication overdose (cholinergic crisis) and underdose (myasthenic crisis) Instruct the client to take medications on time to prevent weakness, because weakness can impair the clients ability to breath and swallow Instruct the client to take the medication before meals for best absorption
TENSILON TEST

tensilon is injected by IV The Tensilon test can cause ventricular fibrillation and cardiac arrest Atropine sulfate is the antidote for overdose Diagnosis of myasthenia gravis: Most myasthenic clients will show a marked improvement in muscle tome within 30 to 60 seconds after injection, and the muscle improvement lasts for 4 to 5 minutes Diagnosis of cholinergic crisis (overdose with anticholinesterase) or myasthenic crisis (undermedication)
TENSILON TEST
In cholinergic crisis, muscle tone does not improve after the administration of Tensilon, and muscle twitching may be noted around the eyes and face A Tensilon injection makes the client in cholinergic crisis temporarily worse (negative Tensilon test) A tensilon injection temporarily improves the condition when the client is in myasthenic crisis (positive Tensilon test)
ANTIPARKINSONIAN MEDICATIONS
restore the balance of the neurotransmitters acetylcholine and dopamine in the central nervous system (CNS), decreasing the signs and symptoms of Parkinsons disease
DOPAMINERGIC MEDICATIONS
stimulate the dopamine receptors increase the amount of dopamine available in the CNS or enhance neurotransmission of dopamine Contraindicated in cardiac, renal, or psychiatric disorders Levodopa taken with a monoamine oxidase inhibitor (MAOI) antidepressant can cause a hypertensive crisis
MEDICATIONS TO TREAT PARKINSONS DISEASE

Medications affecting the amount of Dopamine Amantadine (Symmetrel) Bromocriptine (Parlodel) Carbidopa-levodopa (Sinemet) Anticholinergics Benztropine mesylate (Cogentin) Biperiden hydrochloride (Akineton) Trihexyphenidyl hydrochloride (Artane) Antihistamine Diphenhydramine hydrochloride (Benadryl)
SIDE EFFECTS

Dyskinesia Involuntary body movements Nausea and vomiting Urinary retention Constipation Dizziness Orthostatic hypotension Confusion Mood changes Hallucinations
IMPLEMENTATION
Instruct the client to take the medication with food if nausea and vomiting occur Assess for signs and symptoms of parkinsonism, such as rigidity, tremors, akinesia, and bradykinesia; a stooped forward posture; shuffling gait; and masked facies Monitor for signs of dyskinesia Instruct the client to change positions slowly to minimize orthostatic hypotension
IMPLEMENTATION
Instruct the client to avoid alcohol Inform the client that urine or perspiration may be discolored and that this is harmless, but it may stain the clothing When administering levodopa, instruct the client to avoid excessive vitamin B6 intake to prevent medication reactions
ANTICHOLINERGIC MEDICATIONS
block the cholinergic receptors in the CNS, thereby suppressing acetylcholine activity reduce the rigidity an some of the tremors but have a minimal effect on the bradykinesia Contraindicated in clients with glaucoma
SIDE EFFECTS
Blurred vision Dry mouth and dry secretions Increased pulse rate Constipation Urinary retention Restlessness and confusion Photophobia
IMPLEMENTATION
Assess for risk of injury Encourage the client to avoid alcohol, smoking, caffeine, and aspirin to decrease gastric acidity Instruct the client to minimize dry mouth by increasing fluid intake and by using ice chips, hard candy, or gum Instruct the client to use sunglasses in direct sun because of possible photophobia
ANTICONVULSANT MEDICATIONS
Used to depress abnormal neuronal discharges and prevent the spread of seizures
ANTICONVULSANT MEDICATIONS
Phenytoin (Dilantin) Carbamazepine (Tegretol) Lorazepam (Ativan) Valproic acid (Depakene)
IMPLEMENTATION FOR CLIENTS ON ANTICONVULSANTS

Initiate seizure precautions Monitor urinary output Take anticonvulsant with food to decrease GI irritation, but avoid milk and antacids, which impair absorption Do not discontinue medication Urine may be a harmless pink-red pr red-brown color Report symptoms of sore throat, bruising, and nosebleeds, which may indicate a blood dyscrasia
SIDE EFFECTS

Gingival hyperplasia Reddened gums that bleed easily Slurred speech Confusion Depression Nausea and vomiting Constipation Headaches Blood dyscrasias: decreased platelet count and decreased white blood cell count (WBC) count Elevated blood glucose Alopecia Hirsutism
IMPLEMENTATION
When administering phenytoin, dilute in normal saline, because dextrose causes the medication to precipitate Instruct the client about the importance of good oral hygiene and regular dental examination
BARBITURATES
used for tonic-clonic seizures and acute episodes of seizures resulting from status epilepticus
Barbiturates Phenobarbital
SIDE EFFECTS
drowsiness dizziness hypotension respiratory depression tolerance to medication
BENZODIAZEPINES
-
to treat absence seizures
Diazepam (Valium) used to treat status epilepticus, anxiety, and skeletal muscle spasms Clorazepate (Tranxene) is used as adjunctive therapy for partial seizures
Side effects ataxia respiratory and cardiac depression medication tolerance and drug dependency
BENZODIAZEPINE
Diazepam (Valium) Lorazepam (Ativan)
CENTRAL NERVOUS SYSTEM STIMULANTS
used to treat narcolepsy and attention deficit hyperactivity disorders used to treat respiratory depression used as adjunctive therapy for exogenous obesity
SIDE EFFECTS

irritability restlessness tremors insomnia heart palpitations tachycardia hypertension dry mouth anorexia weight loss diarrhea or constipation impotence dependence and tolerance
IMPLEMENTATION
1. Monitor vital signs 2. Assess mental status 3. Instruct the client to take the medication before meals 4. Instruct the client to avoid foods and beverages containing caffeine to prevent additional stimulation
IMPLEMENTATION
5. Instruct the client not to discontinue the medication abruptly 6. Instruct the client to take the last daily dose of the CNS stimulant at least 6 hours before bedtime to prevent insomnia
NARCOTIC ANALGESICS
suppress pain impulses but can suppress respiration and coughing by acting on the respiratory and cough center in the medulla of the brainstem
NARCOTIC ANALGESICS
Codeine sulfate effective cough suppressant at low doses can cause constipation
Hydromorphone hydrochloride (Dilaudid) can decrease respiration can cause hypotension
NARCOTIC ANALGESICS
Meperidine hydrochloride (Demerol) used for acute pain and as a preoperative medication contraindicated in head injuries and increased intracranial pressure, respiratory disorders, hypotension, shock, severe hepatic and renal disease, and in clients taking monoamine oxidase inhibitors should not be taken with alcohol or sedative hypnotics because it may increase the CNS depression
MEPERIDINE HYDROCHLORIDE (DEMEROL)

Side effects Respiratory depression Hypotension Tachycardia Drowsiness Constipation Urinary retention Nausea Vomiting Tremors
NARCOTIC ANALGESICS
Morphine sulfate
used for acute pain resulting from myocardial infarction (MI) or cancer, for dyspnea resulting from pulmonary edema, and as a preoperative medication contraindicated in severe respiratory disorders, head injuries, increased intracranial pressure, severe renal disease, or seizure activity
preferable for treating the pain of an MI because it reduces the oxygen needs of the heart without reducing blood pressure
Nalbuphine hydrochloride (Nubain)
MORPHINE SULFATE
Side effects Respiratory depression Orthostatic hypotension Urinary retention Nausea Vomiting Constipation Cough suppression Reduction in papillary size Miosis
IMPLEMENTATION FOR NARCOTIC ANALGESICS
Administer medications 30 to 60 minutes before painful activities Monitor respiratory rate, and if the rate is less than 12 breaths per minute in an adult, withhold the medication unless ventilatory support is being provided Auscultate breath sounds because narcotic analgesics suppress the cough reflex
IMPLEMENTATIONS
Have naloxone (Narcan) available for overdose Monitor for pupil changes because pinpoint pupils indicate morphine overdose Note rate and depth of respirations Avoid alcohol or CNS depressants because they can cause respiratory depression
NARCOTIC ANTAGONISTS
used
to treat respiratory depression from narcotic overdose
Implementation Auscultate breath sounds Have resuscitation equipment available do not leave the client unattended Monitor the client closely for several hours because when the effects of the antagonist wears off, the client may again display signs of narcotic overdose
NARCOTIC ANTAGONISTS
Naloxone hydrochloride (Narcan) Naltrexone (ReVia)
OSMOTIC DIURETICS
increase osmotic pressure of the glomerular filtrate, inhibiting reabsorption of water and electrolytes used for oliguria and to prevent renal failure used to decrease intraocular pressure in narrowangle glaucoma used to decrease intracranial pressure
OSMOTIC DIURETICS
Mannitol (Osmitrol) Urea (ureaphil)
SIDE EFFECTS
fluid and electrolyte imbalances pulmonary edema from the rapid shifts of fluid nausea and vomiting tachycardia from the rapid fluid loss hyponatremia and dehydration
IMPLEMENTATION
Monitor lungs and heart sounds for signs of pulmonary edema Change the clients position slowly to prevent orthostatic hypotension Monitor for crystallization in the vial of mannitol prior to administering the medication; if crystallization is noted, do not administer the medication

Nervous System LECTURE

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Nervous System LECTURE

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STRUCTURAL CLASSIFICATION OF THE NERVOUS SYSTEM :

FUNCTIONAL CLASSIFICATION OF THE NERVOUS SYSTEM :

Endorphines & Enkephalins

Name / Number X - Vagus

Composition & Function

XII - Hypoglossal Motor tongue movement Sensory muscles of the tongue

Decreased sense of smell

Is often accompanied by impaired taste and weight loss

DYSFUNCTION Hearing loss, imbalance, vertigo, tinnitus

Dysarthria, Dysphagia, cardiac and respiratory instability

Maintain airway. Prevent aspiration. Swallow therapy

SPINAL NERVE PLEXUSES

Important Nerves Femoral

Important Nerves Superior & Inferior Gluteal

Body Areas Served Gluteus muscles

AUTONOMIC NERVOUS SYSTEM

EFFECTS OF THE ANS

Adrenals Liver Lungs Heart

No effect No effect Bronchoconstriction Dereased HR, slows and steadies

Relaxes sphincters (allowing voiding) No effect

Arrector Pili Muscles

(4) (3) (2) (1)

(6) (5) (4) (3) (2) (1)

(5) (4) (3) (2) (1)

SKULL AND SPINAL X-RAY

COMPUTED TOMOGRAPHY (CT) SCAN

MAGNETIC RESONANCE IMAGING (MRI)

AMERICAN DREAM REVIEW INSTITUTE

obtain a consent have the client empty the bladder

IMPLEMENTATION DURING THE PROCEDURE

CALORIC TESTING (OCULOVESTIBULAR TESTING)

AMERICAN DREAM REVIEW INSTITUTE

NURSING INTERVENTIONS PREOPERATIVE

NURSING INTERVENTIONS: POSTOPERATIVE

NURSING INTERVENTIONS: POSTOPERATIVE

NURSING INTERVENTIONS: POSTOPERATIVE

Signs and symptoms:

absorption of CSF Overproduction of CSF

Two types: Non-communicating

Two types: 1. Non-communicating

Hydrocephalus in utero or infancy or before cranial suture fusion

of moist heat facial massage facial exercise

Two Major Categories: 1. Ischemic / Non - hemorrhagic Stroke

STROKE: RISK FACTORS

Maintain proper positioning, body alignment & skin integrity:

Maintain adequate elimination:

3 Categories of Fluent Aphasia

Expressive or non-fluent aphasia

ANEURYSMAL SUBARACHNOID HEMORRHAGE

are asymptomatic until rupture and produce symptoms of hemorrhagic stroke

ARTERIOVENOUS MALFORMATION Hemodynamic effects

ANEURYSMAL SUBARACHNOID HEMORRHAGE

ANEURYSMAL SUBARACHNOID HEMORRHAGE AND ARTERIOVENOUS MALFORMATIONS

ANEURYSMAL SUBARACHNOID HEMORRHAGE

with cerebral ischemia, hydrocephalus, hypothalamic dysfunction, and seizure activity

OTHER TYPES OF DEMENTIA

OTHER TYPES OF DEMENTIA

OTHER TYPES OF DEMENTIA

OTHER TYPES OF DEMENTIA

OTHER TYPES OF DEMENTIA

OTHER TYPES OF DEMENTIA

Principal pathologic feature:

The Five (5) Cs of Alzheimers Management:

Abdominal cramps, diarrhea, N&V, excessive salivation, excessive sweating