DISEASE INFECTIOUS MENINGITIS

CAUSE Inflamm of the meninges, the protetive membrane lining of the brain and spinal cord Inflame of pia mater & arachnoid of brain and SC Bacterial & viral/fungal protozoal

ADDITIONAL INFO PRED FACTORS: fractures, surgery, sinus & URTI, compromised immune system TRANSMISSION: direct contact; droplet PREVENTION: Immunixation CLASSIFICATION: Aseptic/viral meningitis- cause is viral (leukemia, brain abscess) Septic meningitis- caused by bacteria (N. meningitidesm H. influenza, streptococcus pneumonia)

MANIFESTATION Initial manifestations: headache, fever Classical Manifestations: nuchal rigidity, (+) Kernig s sign (knee), (+) Bruzinski s (head), Photophobia, Optisthatonus (arching of the back) Others: Disorientation and memory impairment, lethargy, unresponsiveness and coma may develop as illness progresses, seizures (sec to focal areas of cortical irritability), inc ICP (sec to accumulation of purulent

DIAGNOSIS Lumbar puncture: Inc in CSF Pressure (cloudy & milky white) Inc CHON level Dec glucose concentration (+) Gram stain, C & S (except in viral) CT Scan/ skull Xra- rule out underlying cause Cultures of blood, urine and throat infection

TREATMENT MEDICATIONS Early admin of antibiotic anti-fungal= (Amphotericin B) Adjunctive therapy (Dexamethasone) Dehydration and shock are treated with fluid volume expanders Seizures are controlled with phenytoin (Dilantin)

NUR MGT Neuro status and VS continually assessed Protect client from injury (seizures or altered LOC) Preventing complications Instituting droplet precaution until 24hrs after the initiation of antibiotics Isolation Precautions Stool & Urine precaution for Viral Meningitis Respiratory isolation: pneumococcal meningitis Proper positioning: HOB elevated 30 degress Avoid hip and neck flexion Opisthotonus: sidelying position Quiet. Non-stimulating enbv t Analgesics, ATB as prescribed

INFECTIOUS: BRAIN ABSCESS

a collection of either encapsulated or free pus within the brain tissue (temporal lobr, cerebellum, frontal lobes) Frontal lobe: most common site A collection of infectious material within the tissue of the brain Arising from a primary focus elsewhere (eg ear, mastoid sinuses, nasal sinuses, heart, distal bones, lungs or primary bacteremia)

CAUSES: Bacteremia, Bacterial Endocarditis Cranial Trauma HIV infection Cranial infection Teeth abscess

Headache Change in mental statis (lethargic, confused, irritable or disoriented) Fever (may not be present)

CT Scan\Arteriography LP can confirm infection but too risky as it can release ICP cerebral herniation CT-guided stereotactic biopsy to drain & culture the abscess C & S\Skull X-ray Radioisotope scanning

Antimicrobial therapy: Penicillinase-resistant antibiotic (Nafcillin) for 2 wks Corticosteroids Osmotic diuretics Antiseizures meds Surgical aspiration or drainage of abscess Delayed until abscess becomes encapsulated Palliative & supportive care

RABIES

Caused by virus transmitted by the bite of a rabid animal Severe inflamm of brainstem & basal ganglia Incubation period: 1-3 months Acute CNS Infection Fatal unless treated promptly Always suspect rabies in any person who suffers an unprovoked animal bite

PATHOPHY: Enters skin & mm replicates in striated muscle at bite site nerves CNS replicates in the brain nerves other tissues including salivary glands RISK:r/t bite location Face-60% UE: 15-20% LE:10% STAGES: Prodromal: Areas of bite: local radiating pain or burning, sensation of cold, prupritus and tingling. Malaise, slight fever, anorexia, nausea, sore throat, persistent loose cough, nervousness, anxiety, irritability, hyperesthesia, photophobia, pupil dilation excessive salivation, tachycardia, shallow respiration Excitation: 2-10 days after prodromal Agitation, marked restlessness, CN dysfunction: Strabismus, anisocoria, absence of corneal reflex, weak facial muscle, hoarseness Pharyngeal spasm & excessive salivation Hydrophobia dehydration Terminal phase Flaccid paralysis vascular collapse coma death

Headache, fever, seizure, hyperirritability, seizures Diff swallowing and foaming in the mouth Respiratory failure occurs

Virus isolation from patient s saliva Blood exam for FRA (Fluorescence Rabid antibody) Confinement of suspected animal for 10 days Observation: of rabid, killed and brain tissue tested for FRA and Negri bodies

Prevention: Prophylactic vaccine Immediate cleansing of the wound and anti-rabies infections

Immediate: wash bite & scratch with soap and water for 10 mins flush with betadine rinse with water Don t immediately stop bleeding may help clean wound Pt w/o immunization with Rig and active immunization Isolate pt Keep room & dark Wear gown, gloves and protection from eyes & mouth when handling saliva and contaminated articles Avoid being bitten during excitation stage

INFECTIOUS ENCEPHALITIS

Severe inflamm of brain Acute inflame process of brain tissue HSV 1 is the most common cause of acute encephalitis (herpes encephalitis) Temporal lobe is the most common site Causes: mumps

Coma for days and weeks, fever, headache, meningeal irritation, vomiting, neuronal damage

C & S blood & CSF Virus speacofooc: indirect fluorescent antibody assays LP: inc pressure, blood glucose normal

acyclovir for herpes encephalitis, anticonvulsant IV, IV Mannitol & corticosteroids, sedative, analgesics & antipyretics,

prvx dehydration, antibiotics for assoc infection, isolation is unnecessary, supportive care

TETANUS

Potentially deadly NS disease due to the bacteried Clostridium Tetani Spores of C. tetani live in the soil In spore form, C tetani may remain inactive in the soil, but can remain infectious for more than 40 yrs. Lockjaw Can thrive in a puncture wound

Can thrive in a puncture wound Exotoxin enters nervous system muscle spasm Jaw stiffnes, diff swallowing, stiff neck, HA skeletal muscle spasm, and respiratory failure Spores enters body thru wound spores release active bacteria spread and meake a posion: tetanospasmin blocks nerve signals from SC (KULANG) POSSIBLE CMPLXS: Airway obstruction, repiratory arrest, heart failure Pneumonia, fractures, brain damage due to lack of oxygen during spasms PREVENTION: Tetanus is completely preventable by active tetanus immunization, immunization is throught toprovide protection for 10 years Nonparalytic doesn t lead to paralysis; abortive typr Causes same mid-flu-like signs ad symptoms; most people recover from this polio in les than a week Genrally last for 2-10days Fever, headache, vomiting, diarrhea, fatigue, back pain or stiffness, neck pain, pain in arms, straight leg raising less than 90 degrees Muscle spasms Paralytic fewer than 1% infected with poliovirus develop paralytic polio most serious form Oropharynx digestive tract blood CNS-> respi failure and paralysis Highly contagious thru direct contact

spasm and tightening of the jaw muscIrritability Fever Addt l sx assoc with excessive sweating, naglalaway dionle (lockjaw) Stiffness and spasms of muscle groups:neck, chest, abdomen, back muscles Titanic seizures

medicine to reverse posion (tetanus immunoglobulin) ATB: penicillin and clindamycin Surgery to clean wound and remove the source of the poision (debridment) Muscle relaxers such as diazepam

Bedrest with a nonstimulating env t (dim light, reduced noise and stable temp) Sedatives, repiratory support with Oxygen, endotracheal intubation

POLIOMYELITIS

Polio or infantile paralysis Acute communicable disease caused by the polio virus and ranges in severity fatal paralytic illness

begins with fever Five days after: headache, neck and back stiffness, constipation, inc sensitivity to touch No force in muscle, pag hinawakan, babaggsak yan Paralytic may be divided in two form: Spinal poliomyelitis: weakness of muscles supplied by spinal Bulbar: weakness of muscles supplied by cranial nerves; encephalitis sx Diplopia, wakness of mastication, diff to chew, nasal voice, dysphagia, respiratory problem, neck drop (paralysis of neck flexers) relate to region affected: diplopoa, scotoma, blindness, muscle spasm, weakness, fatigue, paresthesia, inc susceptibility to infection, infection instability, euphoria during remissions, depression, DYSPHAGIA, ATAXIC GAIT

no cure

palliative & supportive, ATB, analgesics for pain, portable ventilators to assist breathing, moderate exercise, liquid baby foods, juice, lactose, vits, rehab, emotional support

AUTOIMMUNE MULTIPLE SCLEROSIS

Immune-mediated progressive demyelinating disease of the CNS

Incidence: young adults (20-40yo). 3 women to every men, 5 whites for every non-whites Autoimmune Charac by exacerbation and remission (aggravated by fatigue & emotional disturbances) Demyelinating disease of CNS inflamm and destruction of the myelin sheath (irreversible and progressive) Sclerotic plaque(scar tissue) irritation slowing down of impulses

muscle relaxants: baclofen Amantadine(symmetrel): tx of fatigue Methyphenidate (Rifalin) CNS stimulant reduces fatigue Fluoxetine (Prozac): antidepressant Steroids: prevent edema formation, at the sclerotic plaques. Most effective Tx for acute exacerbations Glucoccorticoids: prednisone, Dexamethasone, corticotrophin Vit. B-supports cell replication, enhances metabolic fxns Immunomodulating agents: ABC tensilon test (Edrophontum Chloride test)-- > pag meron, lalakas yung patient because of tensilon injection Short acting acetylcholine (520 mins) plasmapheresis (bsta autoimmune) Thymectomy cholinergic/anticholinesterase (tigmine) admin med on time, give 30 mins before meals with milk crackers, note for over dosage and under dosage SE (dosage): seating, salivation, nausea, salivation, abdominal cramps, bradycardia, and hypotension Glkucocorticoids, antacids Myasthenia crisis: underdosage, infection, stress or fatigue Tx: inc anticholineterase dose Cholinergic crisis: ovedosage Differentitates by a negative tensilon test (sx worsen with tensilon admin) Signs very similar to those myasthenia crisis except hypotension and bradycardia Tx: Atropine Sulfate

eye patch for diplopia, high fiber to pvx contstipation, maintain optimal fxn Physical and speech therapy, force fluids, avoid hot baths, plasmapheresis remove the autoantibodies

MYASTHENIA GRAVIS

Autoimmune disease causing disturbances in transmission of impulses from nerves to muscles resulting in extreme muscle weakness

Acetylcholine receptors destroyed dominant yung dopamine more on suppressing na dahil sa dopamine Overactive thymus gland Acetylcholine: neurotransmitter that stimulates muscle contraction Fewer receptors are available for stimulation, resulting in VOLUNTARY MUSCLES weakness that escalates with continued activity Weakness progfresses

muscle weakness, dyspnea, dysphagia, dec physical activity, fatigue. Ptosis, diplopia, impaired speech, strabismus, snarl smile Mask-like facial expression Drooling Respi difficult, diminished breath sounds

monitor respi status, speech & swallowing abilities Assess gag reflex before feeding the client Admin meds before meals to pvx aspirationprotect from falls, adequate ventilation, avoid exposure to infection, observe for myasthenic & cholinergic

GUILLAINE-BARRE

Rapidly progressing autoimmune attack of the

Resolves about a month after onset of symptoms due to regeneration of myelin sheath

Muscle weakness Diminished reflexes of the lower

Medical emergency: ICU Mgt Assess changes in motor weakness and repi fxn

SYNDROME

peripheral nerve myelin reversible

Also known as: post infectious polyneuritis Progressive weakness and paralysis begin in the lower extremities and ascend bilaterally including respiratory muscles Cranial involvement (facial nerve) produces diff in swallowing and talking

extremities Quadriplegia Neuromusculo repi failure Paresthesias of the hand and feet Pain related to the demyelination of the sensory fibers Blindness Inability to swallow or clear secretions Instability of the cardiomuscular system CRANIAL NERVE DISORDERS

STEROIDS KULANG Pag GBS kaya magrgenrate unlike that on Multiple sclerosis, tsaka peripheral nerves yung naapektuhan

TRIGMENIAL NEURALGIA

Condition of the 5th cranial nerve charac by unikateral paroxysms of pain in the area innervated by any of the 3 brancshesm but mostly occurs in 2nd and 3rd branches

Pathophy: causes: chronic decompression or irritation of the trigeminal nerve Dx: based on charac behavior: avoiding stimulating trigger points Mfx: oain felt on skin (more severe over lip, chin, nostrils, in the teeth) Paroxysms are aroused by stimulation of affected nerve endings (wshing face, shaving, brushing teeth, eating, drinking) Drafts of cold air and direct pressure against the nerve may cause pain Forever ng anjan Pathophy: inflame reaction of 7th cranial nerve around audioty meatus conduction block inhibits neural stimulation of the muscle fibers distortion of face, increase lacrimation Painful sensation of face, behind ear, in the eye Diminished blink reflex Speech inabilities, dysphagia

Anticonvulsive agents: laging ON TIME Carbamasepine (tegrefol) Pheytoin Injection of alcohol Surgery: trigeminal ganliolysis, microvascular gecompression of the trigeminal nerve

assist patient to recognize factors that triggerfacial pain use cotton pads and room temp water Rinse mouth if toothbrushing causes pain Take food & fluids @ room teemp, chew on unaffected side, ingest soft foods Perform personal hygiene pag walang pain

BELL S PALSY

7th cranial nerve (face) that produces unilateral or bilateral facial weakness or paralysis Usually resolves in 3-62wk Cause unknown but may result from: infection, hemorrhage, tumor, meningitis, local trauma

Surgery

maintain facial muscle tone Eye care Steroid therapy, heat therapy, electrical stimulation

PARKINSONS DISEASE (POPE)

Progressive degenerative disorder caused by dopamine depletion. And resulting in a generalized decline in muscular fxn Spams, rigidity

presence of 3 cardinal signs: Tremors Muscle rigidity Bradykinesia

DEGENERATIVE tremors pill rolling, involuntary movt noticeable when extremities are at rest, walking, feeling anxious and concentrating rigidity resistance to passive limb mov t bradykinesia most common sign, has difficulty in initiating mov t; slow mov t hypokinesia abnormally diminished mov t shrinking, slow hand writing dysphonia soft slurred, low-pitched, less audible speech postural and gait problems (stooped posture) diff in pivoting and los of balance

lab imaging not helpful PET scanning for levels of levodopa uptake and conversion Disease is diagnosed clinically from the patient s hx

Stereotatic Trihexyphenidyl HCl MEDS: Amantidine (symmetrel) promotes synthesis and release of dopamine L-dopa precursor of dopa Sinement: converts dopa in CNS Dopamine agonists: -criptine, directly stimulates specific subclasses of dopamine receptors MAOBI inc dopa activity, Selegiline (Elpedryl) ALL ARE USED TO INCREASE DOPA Levodopa most effective -coverted to odpaminein basal ganglia Individualized xare Pharamaco trx mainstream tx Inc dopamine, dec acetylcholine Onhective of therapy: reduce sx Anticholinergic ec involuntary mov t of body (rigidity & tremors) SE: dry mouth, urinary retention, HA, photophobia, constipation

Improve mobility through daily exercise Enhance self care activities Improve bowel elimination Diet: High CHON high Fiber SURGICAL MFX: Neural transplantation of adrenal medullary tissue is performed in effort to restore normal dopamine release Deep brain stimulation- pacemaker like brain implants

AMYOTROPHIC LATERAL SCLEROSIS

Lou Gehrig s disease progressive -unknown cause, loss of motor neuron Iin anterior horns of SC and motor nuclei of the lower brain stem

. Cells die, muscle fibers that they supply uindergo atrophic changes neural degeneration death

Fatigue, progressive MW, cramos, Fasciculation, atrophy of muscles tro the point na wala ng strength, deept tendon refleces become brisk and overactive, diff talking and swallowing, diff in breathing, voice assumes a nasal sound

PHARMS: Riluzole glutamate antagonist that slows deterioration of motor neuron Baclofen muscle relaxants

Monitor respi status. Respi support Do range of motion exercises Life decisions

INCREASE

An increase in ICP caused by trauma,

What happens when ICP rises:

Change in LOC- restlessmess, headache and

Neuromuscular blocking agents as needed

Elevate HOB 15 to 30 deg, avoid trendelenburg

D ICP

hemorrhage, tumors, hydrocephalus, edema or inflammation Intracranial contents: Brain: 1200 cc space CSF: 150cc Blood: 100cc Meninges: 50cc Effects: Impede circulation to the brain Impede circulation of CSF Affect functioning of nerve cells and can lead to brainstem compression Monroe-Kellie hypothesis: Vol of intracranium=vol. of brain + vol. of blood w/in the brain + volume of the CSF w/in the brain Any inc in volume of any of the aboveIncrease ICP

Brain compensates for increases in ICP by: Limiting blood flow to the head Displacing CSF into the spinal canal Increasing absorption or decreasing production of CSF ICP Monitoring- provides data for calculating Cerebral perfusion pressure (CPP) CPP=Mean Arterial Pressure-Intracranial pressure CPP=MAP-ICP MAP=Diastolic pressure +Pulse pressure(systolic-diastolic) /3 Adequate cerebral circulation is ensured if CPP is 70-90mmHg Inc ICP ateempt to normal regulation of ICP Slight inc. in cerebral perfusion pressure If ICP remains high, loss of autoregulatory mechanism passive dilation of cerebral vessels inc blood from venous congestion verbral hypoxia brain death

projectile vomiting Pupillary signs- pressure on oculomotor nervem slower response, pupil inequality, fixed dilated pupils High uncontrolled temperature Blood pressure and pulseinc systolic pressure (vol or resistance) widening pulse pressure slowing of pulse from pressure on vagus nerve CUSHING S TRIAD(above) Respirations Slowing of rate and irregular breathing pattern Focal signs Muscle weakness or paralysis, decreasing response to pain stimulus in comatose patients: (+) Babinski s sign Decerebrate or decorticate posturing Visceral Dec. visual acuity, papilledema (edema of optic disc) Seizures

Ventricular drainage of CSF (Ventriculoperitoneal shunt) Medication include sedatives, osmotic diuretics, corticosteroids, barbiturates Barbiturates dec O2 pvx Inc BP generally not treated unless MAP is >30mmHg or SBP is >220mmHg Enalapril is used: Lowers BP w/o directly dilating cerebral vessels thus preventing vascular induced intracranial HTN Anticonvulsants Hyperventilation with mech ventilator Surgical managements: CSF blockage by placement of shunts Anti-seizure medications used post-supratentorial Craniotomy Supratentorial- HOB elevated Infratentorial- FOB to prevent brain herniation If CSF leakage (basilar fracture). Place pads loosely around ears (otorrhea) and under nose (rhinorrhea) to absorb leaking CSF (Halo sign) and raccoon eyes (parang may black eye) CT scan, MRI, EEG, Cerebral angiography, medical history and neurological examination Lumbar Puncture to rule out any infectious caus Anticonvulsant therapy Dilantin, Tegretol. Diazepam, Phenobarbital Importance of adhering to therapy and maintaining serum levels Avoid alcohol and nicotine Avoid oral thermometers

Keep head in neutral position Avoid flexion/rotation of neck, avoid hip flexion >60 degrees Turn to lateral recumbent position to pvs aspiration Instruct to exhale while turning to pvx valsalvainduced ICP Restrict fluids Monitor VS, electrolyte balance and neuro status Keep env t quiet Schedule procedures to coincide with sedation Avoid activities that ellicit a vasovagal response IV access. F/C, ICP monitoring Neuromuscular blocking agents as needed

SEIZURES

Abnormal excessive discharge of electric activity w/in the brain Epilepsy- disorder characterized by chronic seizure activity- brain or CNS irritation Primary seizure- no identifiable cause Secondary seizure- disease Types: Partial or focal onset- source is localized Simple partial: LOC not affected (90 secs) Complex partial: LOC affected (loss or impaired) (1-2mins)\ Generalized Seizure- source is distributed A partial seizure may spread w/in the brain secondary generalization Generalized seizures are divided according to the effect on body but all involve loss of consciousness Absence(pettimal), tonic-clonic (grandma), myovlonic Focal seizures- confined to specific area Jacksonian-slow clonic mov t in had then to arm then to other side of the body Petit-mal-staring. Tulala, blinking episode 100x/day: common in 4-12 y.o Generalized seizure Generalized tonic clonic seizure (grandma) Most common and best known Begin with stiffening of the limbs (tonic) followed by jerking of limbs and face (clonic) Myoclonic seizures are rapid, brief contractions of bodily muscles. Which usually occur @ same time on both sides of the body Atonic Seizures- abrupt loss of muscle tone Drop attacks, astatic, kinetic sezires, head drops, loss of posture or sudden collapse falls head and facial injuries Use of protective head gear Absence seizures (petitmal) Lapses of awareness, sometimes with staring, that begin and end abruptly, lasting only a few seconds 50 to 100 attacks daily Infantile Spasms

Phases: Prodromal phase- produces aura (sensory signals)- flash of light, mood or behavior changes, sudden sensation of smell or taste: tutumba na and LOC Ictal phase- seizure itself Tonic phase- stops breathing and cyanotic Clonic phase-spasm, severe muscular contraction, drooling of saliva, incontinence, mouth gag Postictal phase- after the seizure; amnesia, confusion, inability to be aroused, sleepiness Status epilepticus- series of generalized seizures that occur without full recovery of consciousness between attacks IV Valium

Note the time and duration of seizure If client is standing, place on the floor, protect head and the body Protect the patient uring the seizure Maintain patent airway Don t insert tongue blade during active seizure Do not restrain Loosen tight clothing DON T SUCTION After seizure Document observation Admin Oxygen; prepare to suction, monitor for incontinence Provide rest and sleep Semi-prone position Stress Reduction Methods

Clusters of quick, sudden mov ts that start bet. 3 mos. AND 2 YRS

CEREBROV ASCULAR ACCIDENT

Destruction of brain cells due to sudden decrease in cerebral blood flow Cerebral anoxia lasting than 10mins causes cerebral infarction with irreversible damage Causes: Thrombosis, embolism, hemorrhage Types: Occlusive strokes- artherosclerotic plaque, an emboli or vasospasm Thrombotic ischemic stroke- partial to complete- TIA Hemorrhagic stroke-ruptured or leaking aneurysm, AVM, bleeding disorder, trauma or arterial rupture

Stages of Development: TIA (transient Ischemic attack) Warning sign of an impending CVA Brief neuro-deficit Visual loss, slurred speech, aphasia, hemiparesis, vertigo 30 sec to 24hrs with complete return to normal Stroke in Evolution Progressive neuro-impairment over a period of several hrs. or days Complete Stroke Neuro deficits remain unchanged it has localized - which side of the brain is affected Health teachings Facial weakness Arm weakness Speech problems Test these symptoms TYPES: Concussion jarring of the brain loss of consciousness few seconds to minute Contusion Bruising to the brain Laceration Bleeding into the brain tissue Epidural hematoma Clot between the skull and the dura laceration of middle meningeal artery Fast; w/ loss of consciousness then with lucid intervals then loss of consciousness again Subdural hematoma Between the dura and the brain Slow, insidious (Acute vs. Chronic) Intracerebral Within the brain TYPES Primary: nagsimula sa brain Secondary: may pinanggalingan Grown in cranial cavity, malignat or benign, primary or metastatic Can compress or invade adjacent tissues- symptoms are caused by the destruction of neurons, inc ICP and displacement of brain structures

Signs and Sx: Depends on the artery affected Vary according to severity of damage and extent of collateral circulation: Increased ICP Symptoms will depend upon which lobe is affected Frontal- speech, motor-mov t, hemiplegia, facial drooping, judgment, personality, thinking and cognition) Parietal-sensory Temporal-hearing, speech Occipital-visual

CT Scan, MRI. LP, Doppler flow studies, EEG and cerebral arteriography

Carotid endarterectomy Surgical evacuation of clot or hematoma Anticoagulants for non-hemorrhagic strokes Anticonvulsants, diuretics, antihypertensives and analgesics TPA (tissue plasminogen activator)-improves neurologic functioning for thrombotic stije Used within 3-4 hrs after the onset of the symptoms Physical and occupational therapy

Provide emergency care: admin O2 Maintain patent airway, suction prn Bedrest to pvx re-bleeding (common in 1st 2 weeks) Posiyion the client to prevent contractures; turn q2h Sspeak slowly and simply; establish form of communication (expressive/receptive aphasia (expressive can understand but can t express; receptive- can t understand) Monitor ICP, VS, I/O Assess LOC Enteral feeding Avoid liquids-easily aspirated Teach use of assisted devices

HEAD INJURY

Trauma to the skull resulting to mild extensive damage to the brain

Depends on the severity and location of the injury ( motor and sensory changes, papillary changes, reduced LOC and seizures) Signs of increased ICP If CSF keajage occurs the client may experience frequent swallowing, otorrhea and rhinorrhea; racoon eyes (pag may leakage, meaning may butas, prone to infection) (may meningeal inflam na)Nuchal rigidity, airway and breathing irregularities

Skull X-ray, CT Scan of head and cervical spine MRI, LP, cerebral angiography and EEG

Place a cervical collar Conitinuous ICP monitoring Concussion-monitor neuro fxn x 24hrs Contusion- neuro function monitored closely if present, clots removed surgically hematomas evacuated, w/ hydrocephalus- managed with a drain

Monitor VS closely for any inc in ICP Perform neuro statement Monitor respi status and maintain airway Suction PRN-hypoxemia and hypercapnia, inc ICP IVF- slow infusion only; monitor I & O Monitor for diabetes insipidus (kulang anticholinergic hormone, ihi ng ihi) and SIADH (water retention, onti lang urine output) Provide quiet env t Take seizure precautions Provide bedrest w/ proper positioning Prevent complication of immobility Nutritional support (start w/ soft diet)

BRAIN TUMORS

Primary: Gliomas, meningiomas Secondary: breast, colon, lungs READDDD KULANG!!!

CT Scan, EEG, MRI and skull Xray

Surgery, radiation, chemotherapy, decompression of increased ICP with drugs or shunting CSF

Assess neuro status Maintain patent airway Seizure precautions; monitor temp

MS Neuroassessment Get nur hx physical assessment\mental status and speech-bheavior, emotion, LOC, attention span,

Orientation to time, place and person Response to verbal, motor and sensory stimuli (glascow Coma scale) GCS Eye response

4-spontaneous 3-open when name is called 2-painful stimuli 1-no response Verbal 5-oriented 4-disoriented 3-inappropriate 2-incomprehensible 1-no response Motor 6-follows command 5-localizes pain 4-withdrawn from pain 3-decorticate Decorticate posturing Result of lesion of internal capsile or cerebral hemispheres Ptx. Has flexion and internal rotation of arms and wrists and extension internal of rotation of plantar flexion of feet DEcerebrate posturing Lesion of midbrain Extension and external rotation of the arms and wrists and extension plantar flexion of feet Neuroassessment Cranial nerve fxn Assess sensory fxn: Pain, temp, position, sense, touch Vision and hearing Assess motor and muscle function Hemiparesis, note muscle tone and strength, involuntary movements Parkinsons-rest tremors Decerebrate or decorticate posturing Cranial nerves exam Olfactory (I): smell Optic (II): vision Oculomotor (III), trochlear (IV), abducens (VI): eye control Trigeminal nerve (V): sensations of face, mov t of the mouth Facial (VII): Facial muscles Bell s palsy Acoustic nerve (VIII): hearing Glossopharyngeal (IX) vagus (X): palate, uvula Spinal accessory (XI): muscle of shoulders and neck Hypoglossal (XII): tongue Assessment of reflexes Babinski Reflex Dorsiflecion of the ankle and great toe with fanning of other toes Corneal reflex-loss of blink reflex; CN V Gag reflex- loss of gag reflex; CN IX and X Assessment of meningeal irritation Brudzinski s sign- flexion of the head causes flexion of the both thighs to the hip and knee flecion Kernig s sign- (bending of knee) flexion of the thigh and knee to the right angles and when extended causes spasm and pain of hamstring. To conscious patients Doll s eye reflex: (+) normal for unconscious, (-) tuned to left, pumunta din sa left Assessment of LOC Levels: I-Conscious II-Lethargy (Delirium, confused state) III-Stupor (w/ pain stimuli) IV-Coma (w/ deeper pain stimuli) Assessment of VS- monitor for increased ICP Assessment of temp Inc. brain s metabolic rate inc. O2 consumptionChills inc by 20%- fever

Cerebral vasodilation swelling of brainDysfunction of hypothalamus or brainstem Assessment of Respiration Cheyne stokes breathing ng malapit na mamatay Neurogenic hyperventilation Apneustic- matagal na inhalation tapos matagal pa bago mag exhale Ataxic-> completely irrefular breathing Cluster coming in diff rates & rhythm Pupillary size and reaction Normal 2-4mm; brisk and reactive Alterations: slow or fixed, unilateral pupil dilation 3rd CN, midposition, fixed and dilated (midbrain damage) Upper motor neuron lesion: Hyperreflexia Hypertonia Paralysis or Paresis in hemiplegic distribution Atrophy (late sign due to non-use) Lower Motor Neuron Lesion Flaccidity Hypotonia Areflexia Muscle atrophy from denervation Muscle weakness of individual muscles or sets of muscles in the spinal root of PN distribution Extrapyramidal Tract Lesion Rigidity Bradykinesia (Loss of strength) Involuntary rest remors Type Absence (petitmal) Duration 2-15sec Seizure Sx Stare , eyes fluttering, automatism (lip smacking, picking @ clothes, fumbling) Postictal Sx Amnesia for No confusion Resumes activity

Generalized (tonic clonic) grandma

1-2mins

A cry, fall tonicity (rigidity) Clonicity (rigidity)

ONSET SIGNS & SYMPTOMS

INTERVENTIONS

Hemorrhagic Sudden Occurs during awake, morning Severe HA Nausea and vomiting Sx of meningeal irritation Increased restlessness, Confusion, Early instability POOR PROGNOSIS Control HTN: Nipride Control hemorrhage with Vit. K Control increased ICP

Thrombotic/Emboli Gradual During sleep Signs & Sx of Cerebral Insufficiency: Blurred vision Dizziness Light headedness Speech disturbance Cerebral Vasodilators Antithrombotics-Anticoagulants Platelet Deaggregators-Aspirin Thrombolytics: Alteplase **there s only a 3 hr window for treatment

Focal signs (related site of infarction) Hemiplegia Sensory loss Homonymous Hemianopsis Aphasia( common with lect cerebral infarct & right handedness)