DISORDERS OF THE NERVOUS SYSTEM ANATOMY AND PHYSIOLOGY Nervous System i. Central Nervous System 1. Brain 2.

Spinal Cord ii. Peripheral Nervous System 1. Cranial nerves 2. Spinal nerves 3. Autonomic Nervous System Sympathetic Nervous System Parasympathetic Nervous System control all motor, sensory, autonomic, cognitive and behavioral activities link the motor and sensory pathways monitor the bodys processes respond to the external environment maintain homeostasis direct all psychological, biologic and physical activity through electrical and chemical activities Basic structure and function of cells in the nervous system NEURONS basic anatomical and functional unit in the nervous system i. Cell Body major part of the neuron ii. Axon carries stimulus away from the cell body extend a very long way from the cell body and do not branch until the very end axons in the PNS are covered with an insulating lipid layer called MYELIN SHEATH for Rapid conduction of Nerve Impulses Each Axon terminates at a SYNAPSE where neurotransmitters and other chemical substances are released. iii. Dendrites direct impulse toward the cell body, usually extend a short distance from the cell body b. GLIAL Cells supportive structures of the nervous system that nourish, support and protect the brain neurons. there are 4 main types of glial cells in the CNS and 1 in PNS because these cells divide by MITOSIS, they are a source of primary TUMORS of the NS. 1. ASTROCYTES star like cells that provide nutrition to neurons, regulate synaptic connectivity, remove cellular debris and control mevements of molecules in the blood brain barrier. 2. OLIGODENDROCYTES produce the myelin sheath within the CNS that insulates the neuron allowing for fast transmission of nerve impulses. 3.EPENDYMAL Cells line the ventricular system and the choroid plexus. They produce CSF and act as barrier between the fluid filled ventricles and cerebral tissue. 4. MICROGLIA small phagocytic cells scattered in the CNS that disintegrate and remove cellular debris and waste products 5. SCHWANN cells cells in the PNS that produce insulating Myelin Sheaths, just as oligodendrocytes do in the CNS, which facilitates rapid conduction of nerve impulses. THE CENTRAL NERVOUS SYSTEM BRAIN 2% of the total body weight Cerebrum - the largest division, composes the top of the brain - enables the individuals to reason, function intellectually, express personality and mood, and interact with the environment - gives intelligence and complex behavior, conscious thoughts and actions A.corpus callosum joined the two hemisphere at the lower portion of the great longitudinal fissure; responsible for transmission of information from one side of the brain to another. B. gyri folded layers or convolutions causing a wrinkled appearance of the cerebrum (grooves and bulges) C. White Matter makes up the innermost layer; contains nerve fibers and neuroglia (support structures) D. Gray matter contains the external or outer portion of the cerebrum which contains billions of neurons (cell bodies); referred to as the cerebral cortex. E. Pairs of Cerebral Hemispheres

- The right hemisphere generally controls the left side of the body and the left controls the right side of the body; usually one hemisphere is considered dominant. 1. Frontal Lobe performs high level cognitive function, has memory storage, influences somatic motor control, controls voluntary eye movements and controls motor aspect of speech in the brocas area. - thought area, speech area, area for learning abilities, area for intelligence and personality (basic attitudes, sense of humor, motivation) BROCAs Area usually found in the dominant area - speech association area that participate in word formulation 2. Temporal Lobe located behind the frontal and under the parietal lobe - plays a Primary role in CEREBRATION (posturing) - contains primary auditory receptive areas and the auditory association area WERNICKEs area responsible for interpreting speech; found in the dominant area of the brain - also contains the interpretative area that integrates somatic, auditory and visual data (impacts perception, learning, memory, emotions and intellectual abilities) 3. Parietal Lobe holds the primary sensory cortex and sensory association areas; in these areas, sensations such as size, shape, weight, texture and consistency are defined and localized. - sensory lobe/ touch area/ movement area (volumtary muscle movements 4. Occipital Lobe visual center for the eyes controls both eye reflexes and interpretation of sight F. Diencephalons (Interbrain) 1.Thalamus relay station for all sensation (memory, sensation, pain impulses) except smell; sorts, analyzes and discards nerve messages and relays them from spinal cord and cerebrum (toward the sensory cotex) 2.Pituitary Gland controlled by releasing and inhibiting hormones produced by the hypothalamus. a.Posterior Lobe releases hormones made by the hypothalamus -Oxytocin stimulates contraction of uterus and milk let down reflex -Anti diuretic Hormone promotes retention of water by kidneys b. Anterior Lobe Master Endocrine gland growth hormone growth and metabolism prolactin milk production follicle production of ova and sperm luteinazing hormone ovaries and testes thyroid stimulating hormone thyroid gland adrenocorticotropic hormone adrenal cortex to secrete glucocorticoids 1.Mamillary Bodies reflex center for OLFACTION (sense of smell) 2.Epithalamus 3.Pineal Body part of the endocrine gland 4. Choroid plexus knots of capillaries within each ventricles that forms the CSF 1.Hypothalamus regulates many body functions -regulates the pituitary secretion of hormones -Maintains temperature regulation by promoting vasoconstriction or vasodilation -hunger center involved in appetite control -houses centers that regulates sleep wake cycle, -BP, aggressive and sexual behavior, emotional responses (blushing, rage, depression, panic and fear) -regulates autonomic nervous system Brainstem 1. Reticular Formation diffuse mass of gray matter extending the entire length of the brainstem a. Reticular Activating System (RAS) special group of reticular formation neurons that is responsible for alertness, consciousness and awake/sleep cycles b. Substantia nigra releases dopamine 2. Midbrain connects the pons and the cerebellum with the cerebral hemispheres - contains center for visual and auditory reflexes, Cranial nerve III and IV contains sensory and motor pathways 3. Pons involve in the control of breathing, contains sensory and motor pathways

CN V, VI, VII, VIII 4. Medulla Oblongata contains centers that controls heart rate, BP, breathing, swallowing and vomiting, CN IX, X, XI, XII Cerebellum largely responsible for coordination of movement, balance, position sense and integration of sensory input. Spinal Cord unlike the brain, gray matter is in the center and is surrounded on all sides by white matter. II. a. b. THE PERIPHERAL NERVOUS SYSTEM Cranial nerves numbered in the order in they arise from the brain Spinal Nerves has 31 pairs of spinal nerves -8 cervical, 12 thoracic, 5 lumbar, 5 sacral 1 coccygeal) - each spinal nerves has a ventral and a dorsal root Dorsal roots sensory; transmits sensory impulses from specific area of the body to the dorsal root ganglia and then sent to the brain. Ventral roots motor; transmits impulses from the spinal cord to the body Autonomic Nervous system collection of motor nerves, regulate activities of the viscera, smooth muscles and glands to maintain a stable internal environment. sympathetic nervous system active during times of stress such as the FRIGHT, FLIGHT OR FIGHT RESPONSES; increases HEART RATE, BP and vasoconstricts peripheral blood vessels; mediated by NOREPINEPHRINE parasympathetic nervous system conservation, restoration and maintenance system - effects during quiet, non stressful environment, decreases Heart rate, increases GIT activity; mediated by ACETYLCHOLINE D. STRUCTURES PROTECTING THE BRAIN AND SPINAL CORD 1. Skull contains the brain protecting it from injury 2. Spine a flexible column that encloses the spinal cord that provides protection and flexibility 3. Cerebrospinal fluid clear, colorless, odorless solution that fills the ventricular system and sub arachnoid space of the brain and spinal cord; serve as a shock absorber to cushion the brain from injuries caused by movement; contains electrolytes, glucose, protein, oxygen and carbon dioxide 4. cerebral circulation Arteries brain is supplied with blood by two sets of arteries that divide into anterior and posterior circulation (these arteries are thinner, have more internal elasticity and less smooth muscle than the arteries in the rest of the body) Internal and external carotids fed the anterior circulation, including the meninges Two vertebral arteries fed the posterior circulation (cerebellum, brainstem) Circle of willis a ring formed between the vertebral and carotid arteries that provides an alternative route of blood flow if one or more of the four vessels supplying it becomes occluded by vasospasm, an embolus or a thrombus; the frequent site of aneurysms(weakening or bulge in an arterial wall) ii. Venous system vessel walls are thinner than the other veins of the body - dural sinuses collect blood from the brain and empty it into the jugular veins to the heart 5. Meninges cover the brain and spinal cord to protect and support. a. dura matter outermost layer; tough membranous tissue that surrounds and extends into the brain tissue. b. arachnoid membrane lies below the dura and is a network of delicate, elastic tissue that contains blood vessels of varying size - contains the arachnoid villi that absorbs CSF

c. pia matter vascular membrane that covers the entire brain with tiny vessels that extend into the gray matter of the brain. 6. Blood brain barrier formed by endothelial cells of the brains capillaries and astrocyte projections; barrier to macromolecules and many compounds which creates a highly selective barrier that guards the entrance to neurons (by active transport, endocytosis, exocytosis); the barrier is very permeable to water, oxygen, carbon dioxide and glucose PHYSICAL ASSESSMENT OF NEUROLOGIC FUNTIONING A. Mental Status - includes orientation to time, place and person - appearance (dress, grooming and personal hygiene) -behavior and mood (posture, gesture, movement, facial expressions) -speech pattern (clear and coherent) -thought and perception (fixed ideas, illusions, preoccupation, hallucinations, paranoia. Agnosia inability to interpret or recognize object seen through senses ) -Level of consciousness (LOC) alert and responsive, drowsy or stupurous, etc Glasgow Coma Scale an objective measure to describe the LOC based on the clients response in three areas (eye opening response, motor response, verbal response) B. Motor Function -inspect all body muscles for size, tone, movement and strength -compare left and right side for symmetry and equality -assess for tremors (rhythmic movements) and fasciculation (twitching)abnormalities:

c.

Decorticate flexes arms, wrists and fingers with adduction of the upper extremities and extension, internal rotation and plantar flexion of the lower extremities. Decerebrate extends, adducts and hyperpronates arms and stiffly extends legs and plantar flexes feet Flaccidity no response to pain, no muscle tone Ataxia incoordination of voluntary muscle groups

C. Cerebellar examination Balance and coordination ROMBERGs test with feet together and eyes closed; there should be minimal swaying for 20 seconds; screening test for BALANCE Rapid and alternating movements and point to point testing assess coordination D. Sensory function 1 Tactile sensation to discriminate location and type of touch (sharp, dull, vibrating) 2 Position sense/ kinesthesia/ proprioception3 With eyes closed, move clients finger or toe up or down and ask him/her to describe 4 the movement 5 Stereognosis ability of the client to identify a thing placed on the patients palm with eyes closed. 6 Graphesthesia ability of the client to identify a number or letter traced on the palm with eyes closed. 7 Two point discrimination touching client with two simultaneous pinpricks and ask how many pinpricks there were. E.Gerontologic Considerations 1. 2. a. structural changes flexed posture, muscle rigidity, tremors and slowed movements, decreased brain weight, loss of strength. sensory alterations vision and hearing loss (may lead to confusion, anxiety, disorientation)

b. c. d. 3. a. b. c. d. e. f.

decreased temperature regulation (fells cold easily) decreased pain perception ( reaction to pain decreases with age) taste and smell alterations (decreased acuity of taste buds and altered olfactory functioning decreases appetite and a safety hazard. nursing implications adequate lighting without glare large printed materials with contrasting colors orientation to new environment sound enhancement low pitched, clear speaking voice in un unrushed pace reinforcement

a. b. c. d. e. f.

obtain history of metal implants (they are not eligible for MRIs) consent is required (procedure lasts from 30 90 minutes) reassure client that procedure is painless asses for claustrophobia inform client that the machine makes a drum like sound request client to remove credit cards, watches or any metal items

III.DIAGNOSTIC EVALUATIONS A. CSF ANALYSIS (Lumbar Puncture) - introduction of needle into spinal subarachnoid space to assess CSF Nursing considerations: Before and during the procedure a. encourage client to void b. assist client to assume fetal position to widen intervertebral spaces c. Local anesthetic is used to numb the lumbar area. d. Label the specimen collected After procedure a. Lie flat in bed for 6 8 hours (may turn to sides) b. Encourage fluid if not contraindicated c. Observe for change in neurological status d. HEADACHE may develop due to CSF leakage e. Bedrest, analgesics and ice to head B. RADIOLOGICAL STUDIES 1. Cerebral Angiography intraarterial injection of a contrast medium with simultaneous radiographs of head and neck to visualize intracranial and extracranial vessels -can be used to find artero venous malformations and/or aneurysms. Nursing considerations: before the procedure a. explain procedure to the client (a contrast material is injected into femoral, brachial or carotid artery and he/she will experience hot, flushing sensation as the dye is injected) b. check allergy to iodine/seafood c. NPO 4 6 hours d. IVF to ensure adequate hydration e. Pre medicate as ordered f. Obtain consent after procedure a. observe arterial puncture site for bleeding or hematoma (apply pressure dressing or ice pack to the area) b. observe pulse distal to the puncture site (diminished/ absent pulse may indicate blockage of vessel by thrombus or embolus) c. Observe affected limb for color and temperature d. Observe for any change in neurological status e. Bed rest for 12 24 hours keeping the legs extended and immobile for several hours to prevent dislodgement of clot. Force fluids following to aid in excretion of the dye

C. ELECTROGRAPHIC STUDIES 1. Electroencephalography (EEG) - graphical recording of spontaneous electrical impulses of the brain from scalp electrodes. - detects epilepsy, encephalitis and dementia disorders; - important criterion in determining brain death Nursing considerations: a. teach client that the test will not deliver electric shock b. shampoo the hair before the procedure to remove oil/spray and following the procedure to remove residual electrode gel or paste. c. Withhold anticonvulsants and other medications as ordered for 12 24 hours d. Have the client eat regular meals to avoid hypoglycemia that could affect the results. 2. Electromyography (EMG) and Nerve Conduction Velocity (NCV) EMG records electrical activity in muscles at rest, during voluntary contractions and in response to electrical stimulation. NCV records speed of conduction in motor and sensory fibers of peripheral nerves detects neuromuscular disorders; myasthenia gravis, Parkinsons disease Nursing considerations: a. explain procedure to the client (small electrode needle will be inserted into the muscles) b. patient may experience a mild discomfort c. time is approximately 45 minutes for one muscle MEDICATIONS 1. Diuretics draws water from edematous tissue and into the vascular system - reduces cerebral edema ( ICP) by inducing diuresis - relieve thirst. Monitor fluid/electrolytes, BP, HR, RR 2. Corticosteroids (dexamethazone) reduce inflammation thus reduces edema (ICP) 3. Sedatives depress CNS activity 4. Anticoagulants (blood thinners) disrupts coagulation process, time to clot Heparin effect is immediate (antidote protamine sulfate) Warfarin takes 4 5 days to effect (antidote vitamin K) 5. Antconvulsants (phynetoin dilantin) control seizure activity - protect client until the drug is in effect (side rails, maintain airway) side effects: gum hyperplasia (oral care, massage gums, soft bristled toothbrush) sedation, G.I. upset, reddish urine, nystagmus 6. Anti Parkinson drugs (levodopa) - dopamine uptake in the brain (cholinergic agents reduces tremors) 7. Cholinergic agents (neostigmine, prostigmine) - inhibit breakdown of acetylcholine 8. Anti histamine (benadryl) blocks effects of histamine which enhances inflammation - decreases tremor and anxiety; causes sedation and dryness 9. Antipyretic medications control fever (fever cerebral metabolism which causes cerebraldemand and may lead to edema)

f.

2. Computed Tomography Scanning - the brain is scanned in layers for density and digitally converted to images of the layers - painless and readily available; sensitive for detecting bleeding, hydrocephalus and ischemic strokes.. - may be done with or without contrast 3. Magnetic Resonance Imaging (MRI) - the brain is scanned in layers by using a magnet to line up hydrogen atoms and then converts the findings of the scan into images. - effective in detecting soft tissue changes (necrotic tissue, tumors, edema, congenital disorders and degenerative diseases) Nursing considerations:

DISORDERS OF THE NERVOUS SYSTEM A.HEADACHE

actually a symptom rather than a disease entity indicates an underlying intracranial, systemic or psychological disorder

causes: o expanding masses head trauma o intracranial bleeding cerebral hypoxia o inflammation of the meninges o infections of brain and spinal cord o eye, ear or sinus diseases o dilatation blood vessels (HPN)

3. 4.

Headache phase throbbing headache intensifies over several hours headache is severe and incapacitating associated with; photophobia, nausea and vomiting, chills, fatigue irritability, sweating edema Recovery phase pain gradually subsides; any physical exertion may exacerbate headache pain; patient may sleep for extended period

Pathophysiology: pain may emanate from the pain sensitive structures of the scalp, muscles, arteries and veins due to traction or displacement and inflammation or direct pressure on the cranial nerves.

Treatment/Medical management a.propranolol beta-blocking agent that inhibit the action of beta-receptor cell in the heart and brain that control the dilation of bloodvessels. b. ergotamine tartrate acts on smooth muscles, causing prolonged constriction of the cranial blood vessels c. NSAIDs

a. b. c.

Classifications:

a. Cluster headaches - more common in older men, precipitated by alcohol or nitrate, vasodilators or histamines -intense, throbbing, deep, often unilateral pain that begins in infraorbital region and spread to head and neck - associated symptoms: flushing, tearing of the eyes, nasal stuffiness, sweating, swelling of temporal vessels. - treatment: narcotic analgesics, lithium therapy, oxygen inhalation - eliminate the cause b. Tension headache (muscle contraction headaches) - caused by contraction of muscles in the neck and scalp due to emotional/physical stressors - usually bilateral that involves the neck and shoulders - associated symptoms: sustained contraction of the head and neck muscles -treartment:non narcotic analgesics(acetaminophen, propoxyphene) - amitriptyline, antidepressants, muscle relaxants - stress reduction (relaxation technique, exercise, meditation) - apply local heat, massage c. Migraine headaches (vascular headache) - caused by dilatation of blood vessels - strongly hereditary - more common in women often associated with hormonal changes following menstrual cycle - tend to occur with stress or life crisis - one side of the head is more affected than the other that lasts for hours to days - can be triggered by the following: menstrual cycle, bright lights, stress, depression, sleep deprivation, fatigue, overuse of a certain medication foods containing tyramine, monosodium glutamate

Nursing Interventions prevent recurrent episode of headache relaxation technique (stress management) adjust lifestyle to reduce fatigue and exposure to bright sunlight, heat or humidity. . eat small frequent meals to prevent in blood glucose level inform patient to avoid the following foods; chocolate, nuts, onions, food seasoning, alcohol

B. INCREASED INTRACRANIAL PRESSURE (ICP) -prolonged pressure greater than 15mmHg -causes: increase in the bulk of the brain, blood supply, CSF Monro Kellies Hypothesis: because the bony skull cannot expand, when one of the three components expands, The other two must compensate by decreasing in volume for the total brain volume and pressure remains constant. Without such changes, ICP will begin to rise. Compliance ability of the brain to adapt to increasing pressure without increasing its ICP. CSF out of cranium through the spinal canal reduction of blood volume in the brain (autoregulation) displacement of brain tissue into the spinal canal (herniation) Pathophysiology: increase in the bulk of the brain compression of brain structure and blood supply cerebral ischemia cerebral hypoxia necrosis (cerebral infarction) inflammation cerebral edema ICP clinical manifestations: a. early signs 1. blurred vision, decreased visual acuity 2. diplopia 3. headache 4. papilledema (swelling of the optic disk) 5. nausea and vomiting 6. change in LOC 7. weakness in one extremity/ one side of the body b. late signs 1. cushing triad (brain stem herniation) systolic BP while diastolic remains constant reflex bradycardia bradypnea 2. abnormal motor response (decorticate, decerebrate and flaccidity) 3. loss of reflexes (papillary, corneal, gag, swallowing) 4. comatose / death

1. 2.

Clinical manifestations: Prodrome phase occurs hours to days before a migraine attack; depression, irritability, feeling cold, food cravings, anorexia change in activity level, increase urination, diarrhea or constipation Aura phase lasts in less than an hour; may provide enough time for the patient to take prescribed medication to overt the full blown attack visual disturbances/ visual field defects - light flashes and bright spots, hemianopsia -paresthesia numbness and tingling sensation of lips, face and/or hands confusion, drowsiness, dizziness paralysis in extreme cases

Medical Management: restore normal pressure by monitoring ICP, medications, surgery, drainage of CSF from ventricular catheter- drainage catheter is inserted via ventriculostomy into the lateralventricles to monitor ICP and to drain CSF to maintain normal pressure. adequate oxygenation control hypertension restrict fluid intake pharmacotherapy

a. b. c. a. b. c. d. e. f.

Nursing Management: assess neurological status every 1 to 2 hours and report any deterioration maintain airway clearance (semi Fowlers, lateral position or keep flat as prescribed) assess for bladder distention and bowel constipation plan nursing care so it is not clustered because prolonged activity ICP maintain fluid restriction as prescribed keep dressings over catheter dry and change dressings as prescribed (monitor for signs and symptoms of infection meningitis such as fever, chills, nuchal rigidity and increasing headache. use aseptic technique when in contact with ICP monitor) monitor for signs of dehydration provide safety and rest a. padded side rails/ hands in mittens b. minimize environmental stimuli (adequate lighting to prevent visual hallucinations, quite room, limited visitors, speak calmly, group nursing care activities) c. avoid restlessness (maybe due to hypoxia, fever, pain, or a full bladder) adequate airway clearance maintain body temperature make sure bladder is not distended d. maintain skin integrity (turning to sides, skin care, lubrication, massage the area) avoid factors that increases ICP a. nausea and vomiting b. sneezing/ coughing c. valsalva maneuver d. oversuctioning e. restraints f. rectal examination g. enema h. flexion of waist, hip and neck (bending or stooping) educate the family that upsetting the patient may increase ICP. Evaluation: normal ICP is maintained ischemia is minimized airway patency and functional status are maintained.

a. b. c. a. b. c. 2.

Classifications: Linear fracture most common with minimal risk of infection and CSF leakage because the dura remains intact. Generally require bed rest and observation for underlying brain injury no specific treatment is necessary. Comminuted and depressed have a higher risk of brain tissue damage and infection if dura is torn. Require surgical intervention within 24 hours Basilar skull fracture involve the base of the skull and are usually secondary injuries. Do not require surgery unless there is persistent CSF leakage. Regular neurological assessments and observation for meningitis are required. Manifestations (basilar fracture) Battles sign ecchymosis over the mastoid process Hemotympanum blood visible behind tympanic membrane Raccoon eyes bilateral periorbital ecchymosis Rhinorrhea CSF leakage through the nose Otorrhea CSF leakage through the ears Halo sign blood stain surrounded by yellowish stain (in dressing/ bed linens) Nursing management: observe for CSF leakage frequently ( halo sign, rhinorrhea, otorrhea) keep nasopharynx and external ear clean (maintain sterile technique) instruct client and family to go to ER if experiences the following: drowsiness or confusion difficulty waking vomiting, slurred speech prolonged headache blood or clear fluid leaking from ears/ nose stiff neck convulsions Brain Injury has the most important consideration in any head injury - maybe secondary to obstructed blood flow and decreased tissue perfusion. Classifications: concussion temporary loss of neurologic function with no apparent structural damage jarring of the brain maybe so slight to cause dizziness and spots before eyes or severe enough to cause complete loss of consciousness) contusion more severe injury in which the brain is bruised with possible surface hemorrhage patient may lie motionless, faint pulse, shallow respirations, cool pale skin, involuntary evacuation of the bowels and bladder, BP and temperature subnormal intracranial hemorrhage an escape of blood into the cranium most commonly associated with blunt trauma. Results directly from trauma or from the shearing forces on cerebral arteries and veins from deceleration acceleration injuries. Hemorrhage may cause a very slow to very rapid neurological deterioration. Classifications: Epidural hematoma collection of blood in the epidural space between the skull and the dura. Usually develops from a tear in menigeal artery (an arterial bleed rapidly expands, leading to rapid deterioration in neurological status) subdural hematoma collection of blood between the dura and the brain. Usually involves the veins. intracerebral hematoma bleeding into the brain tissue. Can occur anywhere in the brain but is most common in the frontal or temporal lobes. Maybe the result of closed head trauma (MVA)

a. b. c.

C. HEAD TRAUMA (HEAD INJURIES) usually due to motor vehicle crashes (most common), falls, assaults and sports damage to the brain from bleeding and swelling is the major risk ( ICP)

1. 2. 3.

Classification: Scalp injury considered as a minor head injury, most vessels constricts poorly causing the scalp to bleed profusely Skull Fracture a break in the continuity of the skull that occurs with or without intracranial trauma. The force of the impact significantly increases the risk of hematoma formation.


1. 2. 3.

Manifestations: epidural hematoma lose of consciousness then a short period of lucidness followed rapidly by deterioration from drowsiness to coma Headache, fixed dilated pupil on the affected side, hemiparesis, hemiplegia and possible seizures. A surgical emergency (burr holes) subdural hematoma manifestations develops slowly, maybe mistaken for dementia. Slow thinking, confusion, drowsiness or lethargy, headaches and possible seizures. intracerebral hematoma expanding clot may lead to herniation. Headache, decreased level of consciousness, hemiplegia, ipsilateral pupil dilatation Medical management: small hematomas will reabsorb spontaneously and maybe treated conservatively. surgical interventions for epidural and larger subdural hematomas. Less successful for intracerebral heamtoma,because of widespread tissue damage. no medication is given specifically for hematomas. Meds maybe given based on the symptoms presented. ICP monitoring and management (read mgt. for ICP) Nursing Management: (read nsg. Mgt. for ICP) maintain airway clearance and ventilation prevent injury promote adequate nutrition (NGT feeding)

D.CEREBROVASCULAR DISEASE I. any functional abnormality of the CNS (neurologic defecits) that occurs when the normal blood supply to the brain is disrupted. II. The onset maybe rapid or gradual. Risk factors: Hypertension, diabetes mellitus, substance abuse, atherosclerosis, smoking, history, cardiac dse Cause: disruption of blood supply to the brain

Pathophysiology: Disruption of blood supply to the brain (closing of lumen of the vessels) impaired cerebral circulation ischemia cerebral infarction neurological deficits

Classifications: 1. Transient Ischemic Attack (TIA) - brief period of neurological deficits that resolve within 24 hours. - Weakness of the lower portion of the face, fingers, hands, arms and legs, transient dysphagia, sensory impairment. Warning of impending stroke. 2. STROKE / cerebrov ascular accident/ brain attack -refers to a permanent neurological deficits types: a. Thrombotic CVA caused by a thrombus(blood clot), tend to form on atherosclerotic plaque in the larger arteries while the BP is lower(during sleep/rest). Most frequent cause of CVA characterized by gradual deterioration of the clients condition. b. Embolic CVA caused by a traveling blood clot, the 2nd most common cause of CVA, has a sudden onset with an immediate symptoms c. hemorrhagic CVA occurs when a blood vessels ruptures commonly caused by poorly controlled hypertension, ruptured aneurysm, tumors, anticoagulant therapy. FATAL rapidly ICP Clinical manifestations: 1. Carotid Arteries occlusion a. hemiparesis and hemiplegia b. Aphasia loss of ability to use language Brocas aphasia motor or expressive aphasia, affects speech production, - unable to form words that are understandable(single word responses) Wernickes aphasia o sensory or receptive aphasia, affects speech comprehension o -unable to comprehend spoken word, can speak but may not make sense Global aphasia o affects both speech comprehension and production. Apraxia inability to perform known task Agnosia inability to recognize familiar objects seen through the senses Hemianopsia loss of one half of the visual field in each eye. 2. Vertebral artery occlusion a. paresthesia pain in the face, nose or eye b. problems with gait c. dysphagia d. dysarthria

Medical management: a. Thrombolytic therapy for ischemic strokes (CVA caused by thrombus or embolus)tissue plasminogen activator a clot dissolving medication b. anticoagulant therapy, diuretics, anticonvulsants, TPN, NGT feeding, gastrostomy feeding

Nursing management: Improve mobility (encourage active ROM on unaffected side and passive ROM on affected side, change position every 2 hours with lesser time on affected side) Encourage independent self care using the unaffected area (for ADLs) Approach on the side where visual perception is intact. For hemianopsia adequate lighting, provide eyeglasses, turning the head to side to scan the visual field. Promote communication allow client to verbalize no matter how long it takes give simple commends, say one word/object at a time anticipate needs, provide reinforcements if speech success Promote nutrition (TPN, NGT, gastrostomy) give small boluses of foods, sitting while feeding Attain bladder and bowel control (Intake/output monitoring) atonic bladder impaired sensation to bladder filling(catheterization) constipation high fiber diet and adequate fluid intake

exaggerated sympathetic response that occurs in clients with T6 injuries or higher. If not treated promptly and correctly may lead to seizures, stroke or death. can occur when an irritating stimulus is introduced to the body below the level of spinal cord injury. (anything painful, uncomfortable or physically irritating such as bowel full of gas or stool, skin irritations, pressure sores, burns, overfull bladder)

Massive vasoconstriction below the injury, vasodilation above level of injury, bradycardia)associated symptoms of autonomic dysreflexia: - bounding headache - nasal congestion - goose pimples - slow pulse - sweating above the level of injury - restlessness

E. SPINAL CORD INJURY usually due to trauma (MVA, falls, diving, sports) risk factors includes older age, male gender, alcohol and drug abuse 6th, 7th cervical, 12th thoracic and 1st lumbar are commonly affected because it has greater range of mobility. injury affects motor and sensory function at the level of injury and below (perception, sexual function and elimination are also affected) Pathophysiology: Injury to vertebrae (compression, pulling, tearing) Bleeding edema (swelling) hypoxia destruction of myelin and axons spinal cord degeneration at LOI and below (paralysis, loss of reflexes, loss of motor and sensory function, autonomic dysfunction)

Medical management: (to prevent further spinal cord injury) 1. respiratory function is the first priority especially in cervical spinal cord injury (oxygenation) 2. immobilizing the injury a. cervical collar if cervical injury is suspected b. immobilize in a flat, firm surface and transport client as a unit c. do not attempt to realign body parts 3. corticosteroids to prevent secondary cord injury from edema and ischemia 4. skeletal traction stabilization and reduction of dislocations 5. surgical intervention laminectomy

1. 2. 3. 4. 5. 6. a. b.

Nursing management: promote adequate breathing and airway clearance improve mobility by repositioning the patient every 2 hours maintain skin integrity maintain urinary eliminations improve bowel function monitor and manage potential complications of immobility deep vein thrombosis check diameter of thigh and calf, anticoagulation, thigh high elastic pressure stockings, adequate hydration. Orthostatic hypotension dilatation and pooling in abdominal and lower extremity

Clinical manifestations: 1. Spinal Shock temporary loss of reflex function bradycardia, hypotension, flaccid paralysis of skeletal muscles loss of pain, touch, temperature, pressure, visceral and somatic sensations bladder and bowel dysfunction loss of ability to perspire (spinal shock is resolved if REFLEXES returns 2. paraplegia paralysis of the lower portion of the body 3. tetraplegia / quadriplegia paralysis of the arms, trunk, legs and pelvic portion 4. Autonomic dysreflexia

F. SEIZURE DISORDER -sudden abnormal electrical discharges from the brain that results in changes in sensation, behavior, movements, perception or consciousness -maybe due to drug/alcohol withdrawal or traumatic brain injury Epilepsy chronic disorder of recurrent episodes of seizures. -an isolated, single episodes of seizures does not constitute epilepsy - not a disease but a symptom of disorder of brain function - electrical disturbances in the nerve cells of the brain causing them to emit abnormal, recurring, uncontrolled electrical discharges. Cause: unknown in half of all cases The other half is due to: a. genetic disorder or degenerative diseases b. birth trauma inadequate O2 supply, hemorrhage c. infectious diseases meningitis, encephalitis or brain abscess d. ingestion of toxins mercury, lead or carbon monoxide e. brain tumors, head injury or trauma f. stroke hemorrhage, thrombus, embolus

Medical management: 1. pharmacologic therapy - doesnt cure but control seizure activity anti epileptic / anti convulsant meds ( carbamazepine/tegretol, phynetoin/dilantin) 2. surgical management intended for intracranial tumors, abscess, cysts, vascular abnormality Nursing management 1. during seizure activity provide privacy and ease the patient to the floor protect the head with a pad to prevent striking to hard surface loosen constrictive clothing push aside any furniture that may injure the patient avoid restraints if there is an aura, insert an oral airway keep patient on one side to prevent aspiration reorient patient to the environment (after seizure activity) 2. reduce fear of seizures encourage compliance to anti epileptic drugs remove precipitating factors (emotional, environmental, physical) G. MENINGITIS -an inflammation of the meninges in the brain and spinal cord due to infection Risk factors: basilar skull fracture otitis media sinusitis mastoiditis neurosurgery systemic sepsis impaired immune function causes: bacterial, viral, fungal or parasitic causes an inflammatory responses bacterial meningitis: meningococci (niesseria meningitides) common in adults pneumococci ( streptococcus pneumoniae) common in adults haemophilis influenza common in children and young adults These bacterias often present in the nasopharynx

Pathophysiology: Abnormal/ hypersensitive neuron in the brain continue to release electrochemical energy(messages to the body) continue firing of discharges occur even though the task is completed (electrical activity are not controlled and modulated) erratic performance of body parts (controlled by these cells) muscle contraction and possibly loss of consciousness inhibitory neurons interrupts the seizure and causes intermittent contraction relaxation phase epileptogenic neurons becomes exhausted/ inhibitory processes build up (CNS depression and impaired consciousness - sleep, confusion, fatigue) seizure drops

STATUS EPILEPTICUS ongoing seizure, prolonged seizure activity accompanied by respiratory distress (life threatening). Potential complication of seizure. 1. Simple partial sudden, unexplainable feelings of joy, anger, sadness or nausea - may see, hear, taste, smell or feel things that arent there - only a finger of hand may shake, or mouth jerk uncontrollably - for some, a warning sign of impending complex partial seizure 2. complex partial seizure str altered LOC, automatism -repetitive behaviors; chewing, lip smacking, twitching or walking in circle 3. Absence seizure brief change in LOC (less than 20 seconds), mistaken for day dreaming - blinking/ rolling of the eyes, blank stare, slight mouth movement 4. myoclonic seizure loses consciousness for a moment then is confused postictally - brief involuntary muscular jerks of the body or extremities for less than a second 5. generalized tonic clonic seizure (grand mal seizure) - change in LOC, body stiffening alternating between muscle spasm and relaxation - tongue biting, incontinence, labored breathing, apnea, cyanosis - confusion and difficulty talking upon wakening - drowsiness, fatigue, headache, muscle soreness, weakness 6. atonic seizure total loss of muscle tone, leads to injuries due to fall - temporary loss of consciuousness

viral meningitis usually less severe; the course of the disease is usually shorter and benign mode of transmission : direct contact (discharges from the nose and throat) Pathophysiology: nasopharyngeal infection infection extends to the meninges and CSF infection spread quickly to the brain and spinal cord permeability of blood brain barrier cerebral edema increased intracranial pressure cerebral blood flow

Clinical manifestations: 1. nuchal rigidity stiff neck (difficulty flexing the head) 2. (+) brudzinskis sign pain, resistance and hip and knee flexion -occur when the necks flexed to the chest while being supine. 3. (+) kernigs sign pain, resistance on extending the legs 4. photophobia extreme sensitivity to light 5. restlessness, agitation and irritability 6. chills, high fever and malaise 7. severe headache 8. confusion, altered LOC 9. seizures and other signs of ICP

Blood cells are then returned without the plasma to remove antibodies that cause disorder. Complications: watch for bleeding from loss of clotting factors and fluid and electrolyte imbalance. supportive care to maintain function of all body systems (respiratory, cardiac, renal and skin) IV immunoglobulins, corticostereoids

Medical Management: surgical treatment placement of OMMAYA reservoir (to allow intrathecal administration of antibiotics. antibiotic therapy (high dose broad spectrum antibiotics to cross blood brain barrier) chloramphenicol anticonvulsants, antipyretic, analgesics, antiemetic IV fluid replacement

Nursing Management: monitor fluid balance (do not dehydrate or over hydrate) maintain aseptic technique reassurance and support for familys knowledge that signs and symptoms decreases on recovery nsg. Mgt. for ICP

H. GUILLAIN BARRE SYNDROME - an acute , rapidly progressive inflammation of peripheral motor and sensory nerves characterized by motor weakness and paralysis that ascends from lower extremities cause: unknown -autoimmune reaction suspected because it often develops after viral infection, immunizations, fever, injury and sometimes surgery. -Virus: cytomegalo virus, Epstein Barr, campylobacter jejuni (found in poultry, pets and contaminated water. Pathophysiology: Autoimmune response(infection) segmental demyelination of the peripheral nerves (prevents normal transmission of impulses) inflammation and degenerative changes (in spinal nerve roots) sensory and motor deficits/loss (occur simultaneously)

Nursing Interventions: 1. monitor respiratory status (rate, depth, breath sounds, vital capacity, reflexes) - elevate head of the bed (facilitates respiration) - chest physiotherapy and pulmonary hygiene measures 2. Range of motion exercise (to reduce effects of immobility) - DVT, pulmonary embolism, pressure ulcers 3. maintain adequate nutrition as appropriate (enteral/ parenteral nutrition, small frequent feeding of soft foods, weigh client weekly, check electrolyte status) 4. monitor bowel and bladder function - assess bowel sounds and frequency, amount, color of bowel movements - offer bedpan, check for distention, and perform intermittent catheterization PRN 5. eye care provision with client who has inability to close eyelids completely - provide artificial tears, eye shield and tapes 6. promote communication with client and family (especially if on ventilator) - encourage to express feelings and participate as much as possible - relieve fear and anxiety, give positive feedback (recovery is possible proper care)

Evaluation: - client maintains satisfactory respiratory, cardiac, GI and renal status -client resumes ability to move extremities and recover from illness with no permanent loss of function. I. AMYOTROPHIC LATERAL SCLERORIS

progressive physical degeneration while leaving the patients mental status intact a motor neuron disease, increased in middle aged males familial/ genetic with autosomal dominant trait LOU GEHRIGs disease patient is admitted twice (diagnosis and final stage of debilitation)

Clinical Manifestations: 1. symmetrical ascending paralysis - lower extremities and then to total paralysis requiring ventilatory support - paralysis ascends and stays at a maximum level of 2 3 weeks and then slowly descends 2. paresthesias (numbness and tingling sensations) and pain 3. difficulty with extraocular eye movements, dysphagia, diplopia, difficulty speaking 4. orthostatic hypotension (autonomic dysfunction), hypertension, change in heart rate, bowel and bladder dysfunction, flushing and diaphoresis 5. respiratory compromise (dyspnea, diminished vital capacity and breath sounds) Medical Management: plasmapheresis plasma is removed and separated from whole blood.

Pathophysiology:

myelin sheath destruction scar tissue formation distortion/ blocking of nerve impulses the muscle they serve begin to atrophy

1. 2. 3. 4. 5. 6.

Clinical manifestations: progressive muscle weakness atrophy of muscles (muscle wasting) fasciculations (twitching, involuntary muscle contractions) dysphagia jaw clonus dysarthria

7. 8.

difficulty breathing depression (awareness of degeneration) Medical Management: NGT feeding, gastrostomy feeding prosthesis to support weakened muscles Nursing Management: Assist with ADLs promote effective airway clearance promote nutrition (small frequent, high nutrient feeding) emotional support (encourage family to start the grieving process)

4. 5. 6.

avoid fatigue (it can exacerbate the symptoms) improve bowel elimination provide small frequent feeding

K. MULTIPLE SCLEROSIS chronic, degenerative progressive disease of the CNS characterized by demyelination of white matter in the brain and spinal cord. characterized by exacerbations and remissions major cause of chronic disability in young adults cause: unknown, viral infection, defective immune response, genetic Pathophysiology: infection (autoimmune response) attacks white matter of the brain inflammation, edema (destruction of myelin sheath) scarring (hard yellow plaques, gliosis) disruption of nerve conduction neurological dysfunction (depends on the nerve affected) Clinical Manifestations: weakness or tingling sensations (paresthesia) of one or more extremities vision loss, blurred vision, diplopia (optic neuritis) ataxia or incoordination (cerebellum) bowel and bladder dysfunction incontinence, frequency, urgency, infections (spinal cord) depression/ emotional lability mood swings, irritability, euphoria Medical management: no cure exists palliative treatment to delay the progression ofdisease, manage chronic symptoms and treat acute exacerbations; prevent destruction of nerve tissue by suppressing immune system and decrease inflammation. corticosteroids (prednisone) glatiramer acetate reduce frequency of attacks interferons beta 1a or 1b decrease progression, frequency and severity of exacerbations. symptomatic treatment Nursing Management:

J. PARKINSONS DISEASE a slowly progressive disease secondary to degeneration of the basal ganglia in the cerebrum. results from the loss of neurotransmitter dopamine in a group of brain structure that control movements more men than women cause: unknown, genetics, atherosclerosis, viral infection, head trauma, chronic use of antipsychotic meds Pathophysiology: unknown / toxin substantia nigra is destroyed dopamine production imbalance of neurotransmitter (dopamine, acetylcholine) loss of inhibition in the brain parkinsonian symptoms

1.

Clinical Manifestations: tremor slow, unilateral, resting tremor (pill rolling tremor) usually disappear with purposeful movement rigidity stiffness of the neck, trunk and shoulders bradykinesia slowed movement, difficulty initiating movement/ walking mask like and expressionless face frequency of blinking and wide open eyes low pitch monotonous voice drooling dysphagia shuffling gait stooped posture

2.

.promote physical mobility by encouraging exercise with alternating frequent short rest periods to avoid fatigue. preventing injury -patient is at risk to fall (walk with feet apart and assistive device) enhance bladder and bowel control manage speech and swallowing difficulties (suction apparatus readily available) allow independence in self care activities avoid physical and emotional stressors air conditioned room (exposure to heat fatigue and muscle weakness

Medical Management: 1.drug therapy LEVODOPA dopamine replacement, best taken with meals - ensure that patient voids before taking the drug because it causes retention ( UTI) - avoid foods containing vitamin B6 or protein rich foods 2. surgery if drug is ineffective stereotactic surgery uses electrical coagulation, freezing, radioactivity or UTZ to destroy the ventrolateral nucleus of the thalamus to prevent involuntary movement. Nursing management: 1. encourage patient to remain active (slow progression of the disease) 2. encourage independence in ADLs 3. provide a safe environment

L. MYASTHENIA GRAVIS - a disorder affecting the neuromuscular transmission of the (1) voluntary muscles of the body and (2) muscles innervated by cranial nerves (face, lips, tongue, neck and throat) - excessive weakness and fatigability exacerbated by exercise and repeated movements cause: unknown, autoimmune responses, thyroid disorder(thymomas) Pathophysiology: blood cells and thymus gland produce antibody antibody block/ destroy/ weaken neuroreceptors in neuromuscular junction failure in transmission of Ach neurotransmitter to muscles muscular weakness/ paralysis Clinical Manifestations: extreme skeletal muscle weakness and easy fatigability tire on slight exertion, worse after effort (combing, chewing, talking) relieved by rest weak eye closure, ptosis and diplopia (muscles controlling the eye) blank mask like facial expression (facial nerves) difficulty chewing and swallowing (bulbar muscles) hanging jaw bobbing motion of the head

M. ALZHEIMERS DISEASE - senile dementia, chronic, progressive and degenerative neurologic disorder that affects the brain and results in cognitive impairments such as impaired thinking, memory loss and bizarre behavior. Risk factors: family history, aging Cause: unknown, autoimmune deficiencies in neurotransmitter Ach, somatotain, norepinephrine repeated head trauma chromosomal abnormalities deposits of beta amyloid plaques Pathophysiology: neurofibrillatory tangles, amyloid plaques, granulovascular degeneration (three distinguishing features of AD) nerve terminals degenerate (generalized atrophy) memory failure, personality changes and problems carrying ADLs Clinical Manifestations: 1. early signs o forgetfulness/ memory loss o difficulty learning and remembering new information o deterioration in personal hygiene and appearance o inability to concentrate 2. late signs o difficulty with abstract thinking and activities that require judgment o progressive difficulty communicating o severe deterioration in memory, language and motor function o repetitive actions or perseveration o nocturnal wakening, disorientation and personality changes Medical Management: 1. palliative treatment tacrine HCl (cognex) enhances Ach uptake in the brain thus maintaining memory skills antipsychotics, anxiolytics, antidepressants 1. Nursing Management: provide effective communication system with the patient and family -unhurried, clear and easy to understand sentences - reduce noise and distractions - list simple written instructions support cognitive function - quiet, pleasant manner of speaking, clear and simple explanantions - displayed clock and calendars promote physical safety - remove obvious hazards, provide nightlights and avoid restraints provide emotional support to reinforce positive self image promote independence in self care activities provide socialization and intimacy needs - visitors, letters and phone calls (brief and non stressful) - touching and holding expressions of love promote adequate nutrition -offer one dish at a time to avoid playing - serve familiar foods, serve into small pieces to avoid choking promote activity and rest balanced - encouraged participation to activities, provide - music, warm milk, back rub prevent complications -increased susceptibility to infection (pneumonia, UTI, TB, GIT and skin infections -altered pain and febrile response -altered emotional impact (autonomy/ independent decision making)

Medical Management: 1. anticholinesterase agents increases concentration of available Ach at neuromuscular junction a. Edrophonium a short acting drug (+) tensilon test improvement after taking drug then wear off after effect of the drug b. neostigmine methylsulfate (prostigmine) longer duration of effectivity 2. plasmapheresis 3. thymectomy Nursing Management: monitor pulmonary function frequently to detect pulmonary problems encourage rest before becoming too tired

emphasize importance of taking the medications to prevent major complications a. myasthenic crisis caused by undermedication - sudden motor weakness, unresponsive to meds, sudden worsening of the condition - associated with respiratory distress, cyanosis, inability to speak and swallow b. cholinergic crisis caused by overmedication - severe muscle weakness with GIT symptoms - abdominal cramps and excessive pulmonary secretions

2.

3. 4. 5. 6. 7. 8. 9.

improve communication listening to patient, repeat to clarify and verify provide eye care (artificial tears, taping, eye patching) prevent aspiration decreased ability to chew

N. BELLs PALSY

a cranial nerve VII disorder which causes a unilateral paralysis of the facial muscles 80% recover in a few weeks or months (complete recovery) cause: unknown, infection, inflammation, viral, meningitis, hemorrhage Pathophysiology: inflammation around CN VII conduction blockage (CN VII cannot stimulate facial muscles) unilateral facial weakness or paralysis Clinical Manifestations: unilateral facial weakness or paralysis with aching jaw drooping mouth (causes drooling on the affected side) distorted taste perception over affected anterior portion of the tongue inability to close the eyes on the weak side bells phenomenon (eye rolling upward as eye is closed) inability to raise eyebrow, smile, show the teeth on affected side painful sensations in the face, behind the ear and in the eye

1. 2. 3. 4. 5. 6. 7.

Medical Management: 1. administration of corticosteroids 1. 2. 3. 4. 5. 6. 7. Nursing Management: reassure patient that there is no stroke taking place apply moist heat to the affected side of the face to reduce pain massage the patients face with a gentle upward motion (3X daily for 5 10 mins) apply facial sling to improve lip alignment give the patient frequent and complete mouth care protect the eye (wrap around sunglasses/goggles, closed paralyzed eye manually) facial exercise to prevent muscle atrophy -wrinkling the forehead, blowing out the cheeks, whistling