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174 Cards in this Set
- Front
- Back
Essential neural systems |
Arousal and maintenance of attention Memory and language Mood and emotion |
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Full consciousness |
Awareness of self environment and response to environment -Decrease in any of these decreases the LOC Involving arousal and awareness |
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Arousal |
Arousal involves state of Awakening and is mediated by the RAS - cognitive cerebral functions cannot occur without the RAS - vegetative state occurs when cerebral function is lost but Ras and brainstem and maintain a crude awake state |
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Awareness |
Awareness involves the thought process |
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Changes in arousal |
Structural changes, according to location of the condition -Above the tentorial plate: supratentorial involves cerebrum - below the tentorial plate: infratentorial involves RAS or brain stem |
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Structural causes for a change and arousal |
Infection, vascular, neoplastic, traumatic, congenital, degenerative, metabolic |
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Supratentorial |
Changes occur by: - diffuse dysfunction - Encephalitis, neoplasms, close to head trauma leading to subdural hematoma - localized dysfunction - direct pressure on structures, especially Thalamus and hypothalamus |
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Infratentorial |
Changes occur via direct destruction or compression of RAS or brainstem - pressure can be there right or from herniation - examples accumulation of blood or pus - neoplasms or demyelinating disorders |
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Arousal disorders caused by metabolic changes |
Hypoxia, electrolytes disturbance, hypoglycemia, toxins both endo and exo Slight drowsiness to coma exo exo Slight drowsiness to coma Slight drowsiness to coma |
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Psychogenic reasons for arousal disorders |
Not a common cause or physical cause Psychiatric disorder implying unconsciousness, but the person is physiologically awake |
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5 clinical manifestations that Aid in determining the extent of brain dysfunction |
LOC Pattern of breathing Pupillary reaction Oculomotor response Motor response |
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Level of consciousness (LOC) |
Most critical index of CNS function - full orientation: A & O x 3 (p,p,t) - confusion: inability to think rapidly / clearly; impaired judgement - disorientation: time, then place, then self; also memory loss - lethargy: limited spontaneous movement / speech; easy arousal but may not be oriented to p, p, t -obtundation: arousal reduced, limited response to environment - stupor: deep sleep / unresponsiveness; vigorous stimulation to awaken - coma: no verbal response to stimuli; unpurposeful movement may occur - deep coma: no response to stimuli, even deep pain - light coma: purposeful movement with stimulation( withdraw to pain) |
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Patterns of breathing |
Helps determine level of brain dysfunction - normally cerebrum produces a rhythmic pattern - with decreased LOC, lower brain stem takes over - Cheyne - stoke's breathing pattern - responds only to changes in PaCO2 - if ta CO2 increases, tachypnea occurs and PaCO2 drops and drive to breath stops - apnea - PaCO2 rises and it starts over again -Opiate overdose causes decrease in Raitt, consistently - always assess rate, Rhythm and pattern |
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Pupillary response |
-Control for pupils is located near brainstem area that controls arousal - helps determine level of brainstem dysfunction |
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Condition of patient versus pupil response |
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Oculomotor response |
Choose changes at various levels of brain dysfunction in comatose state |
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Metabolic coma |
Ocular reflexes present |
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Barbiturate hypnotic coma |
Ocular reflexes absent |
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Compression to brain stem |
Specific to injury; - Dolls I eye response - normal: eyes turn to side opposite of head movement - ABN: eyes move and direction of head turn - caloric ice water test - normal: both eyes turn toward syringe - ABN: asymmetric or no eye movement |
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Motor response |
Helps determine the level of the brain dysfunction and the most severely damaged side of the brain - responses are categorized as: - purposeful - inappropriate or generalized - absent - four signs primitive reflexes -reflex grasping and suckling -snout reflex -rigidity -vomiting is usually a complex reflex-like motor response -ocuring without nausea indicates central nervous mechanism |
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Outcomes of alterations |
Depends on extent of brain damage and duration of coma -morbidity: extent of disability -irreversible come -vegetative state -minimally conscious state -locked-in in syndrome -cerebral death -mortality rate: death - brain death -cerebral death |
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Possible outcomes of disability |
-rocovery of consciousness -residual cognitive function -psychologic function -vocational function |
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Total brain death |
-can never recover -cannot maintain homeostasis -"irreversible cessation of function of the entire brain including the brainstem and cerebellum" -can pursue legal withdrawal of life support |
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Cerebral death |
-death of cerebrum but not the brainstem and cerebellum -permanent and unable to respond |
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Coma |
Eyes closed, no voluntary movement/speech |
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Persistent vegetative state |
Awareness of self but no cognitive function Sleep/wake with spontaneous eye opening |
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Minimally conscious state |
May follow simple commands, gesture, blinking, smiling, speech |
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Locked-in syndrome |
No voluntary movement except eyes Thought and arousal are intact |
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Alterations in awareness |
Can involve cognitive functions, simple to complex Selective attention deficit Memory deficit: amnesia Executive attention deficits |
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Selective attention deficit |
Inability to select and process information -seizures, parietal lobe confusion, subdural hematoma, stroke, tumor, late alzheimers frontotemporal dementia |
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Memory deficit amnesia |
Retrograde Anterograde |
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Retrograde amnesia |
-Gross loss of past memories or factual data OR loss just prior to the trauma/disease -concussion |
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Anterograde amnesia |
-Can recall distant past but unable to form new memories or retain data since the trauma/disease -Concussion |
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Executive attention deficits |
Inability to maintain sustained attention and a working memory -Cannot set goals, reach goals -Cannot follow instructionsCan be temporary, progressive or permanent -Examples -ADHD can be temporary or continue into adulthood -Depression -Learning disabilities
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Pathophysiology of awareness alterations |
Mechanism involves cell destruction -Ischemia and hypoxia -Effects of toxins and chemicalsManifestations are dependent on the part of the brain involved -Prefrontal area: disorder in vigilance -Parietal lobe: neglect syndrome -Left lateral frontal: memory issues -Cerebral cortex: retrograde amnesia -Hippocampus and temporal lobe: anterograde amnesia -Frontal/prefrontal: executive attention deficitsTreatment -Reverse causes when possible, rehabilitative services concentrating on compensatory measures |
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Seizure disorders |
A syndrome, not a specific disease -Alters the neuronal environment in the brain (seizure threshold) -Hypoglycemia, fatigue, sleep deprivation, emotional or physical stress, fever, low sodium, stimulant drugs, withdrawal from depressant dugs/alcohol, respiratory alkalosis, blinking lights, loud noises, certain odors |
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Seizure |
Sudden disordered discharge of cerebral neurons, temporary altering brain function and level of arousal |
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Convulsion |
Seizure activity in which muscles contract-relax in a tonic-clonic movement |
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Epilepsy |
-More than one seizure, without a correctable cause and will recur without treatment-Metabolic defects, perinatal/postnatal injury, infection, brain tumor, vascular disease, drug or alcohol abuse |
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Types of seizures |
Partial seizures Generalized Unclassified |
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Partial seizure(begins locally) |
-Simple: no LOC-Complex: change in LOC-Secondarily generalized: begins locally but evolves into generalized tonic-clonic |
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Generalized (bilaterally symmetric without local onset) |
-Absence-Myoclonic (shock-like contractions of muscle groups)-Clonic (intermittent muscle contractions and relaxation)-Tonic (muscle contraction)-Tonic-clonic-Atonic (normal tone) |
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Negative consequences of a seizure |
-60% increase in oxygen consumption during a seizure-Cerebral blood blow increases to accommodate-As oxygen and glucose is depleted, lactate accumulates in the brain -Thus the reason to give emergency medications to stop a seizure -If not stopped, brain injury and irreversible damage-Cardiac arrest is also a potential issue |
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Clinical assessment seizure |
-How and where did it start-Was there an aura/prodroma-How long did it last-Did it require medication to stop it-Loss of bowel or bladder-Loss of consciousness-Length of postictal state |
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Diagnosis and treatment - seizure |
Laboratory tests -Blood for glucose, calcium, BUN, creatinine clearance -Urine for sodium level -CSF for infectionCT/MRI -Lesions, fractures, bleedEEG -Type of seizure and if a focus existsTreatment -Correct/ control the cause -Give antiepileptic medications to suppress seizure activity |
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Data processing problems |
Agnosia Dysphasia/aphasia AgnosiaDysphasia/aphasiaAcute confusion (delirium)Dementia Acute confusion (delirium) Dementia |
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Agnosia |
-Inability to recognize shape/form of objects: tactile, visual, auditory-Most common cause is CVA |
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Dysphasia /aphasia |
-Inability to comprehend or produce language -Expressive: inability to communicate needs verbally-Receptive: inability to understand -Echolalia: can repeat clearly but there is no comprehension |
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Acute confusion (delirium ) |
Transient awareness due to cerebral dysfunction -Generally due to drug intoxication/withdrawal, metabolic disease, trauma, nervous system disease, surgeryPathophysiology -Disruption of RAS, affecting cortex and limbic system -Either affects portions of the brain or the neurotransmittersClinical Manifestations -Highly distractible, unable to concentrate on incoming sensory data -Onset is usually abrupt: restless, irritable, poor concentration -Later (2-3 days): illusions, hallucinations and delirium, incoherent -Common in ICU and with withdrawal of CNS depressants -ANS overactivity: cannot sleep, flushed, dilated pupils, tachycardia, increased temp/sweatingTreatment -Determine the cause of the behavior (delirium versus dementia) -Treat the underlying cause and symptoms |
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Dementia |
Progressive deterioration in orientation, memory, language, judgement and decision- making (behavior changes) -Many cerebral functions may be involved -Neuron degeneration -Compression -Atherosclerosis -Trauma -Neurodegenerative diseases (Alzheimer/ Huntington) -Infections, including HIV and slow growing virusesEvaluation and treatment -Rule out other causes; long process -No cure, maximize remaining capacities and work with family |
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Dementia verses delirium |
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Leading cause of dementia |
Most common form is late-onset Alzheimer Dementia -Exact cause unknown, but may be related to chromosome 19 -Brain changes include -Formation of neuritic plaques leading to death of neurons -Neurofibrillary tangles in the cerebral cortex -Degeneration of forebrain cholinergic neurons and acetylcholine -Leads to decline in memory, attention and cognitive functions |
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Clinical manifestations of dementia |
-Early stages usually attributed to something else: illness, forgetfulness-Insidious, with progression of forgetfulness, especially recent events-Disorder advances with disorientation, confusion, loss of problem solving skills -Behavioral problems result: anxiety, depression, agitation, restlessness |
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Alzheimer's Continued |
-If posteriorfrontal lobes are involved, motor function is affected -Rigidity,flexion posturing -Evaluation and Treatment -Diagnosis ofexclusion -History,mental status exam, depression -Treatment -No cure, butsome medications slow the process -Treatment isaimed at compensation of losses -Memory aids -Assistancewith ADLs, especially those requiring cognitionN/ |
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Alteration in Cerebral Hemodynamics |
-Secondarybrain injuries occur after a brain is injured and include alterations in -Cerebral bloodflow -Intracranialpressure -Oxygendelivery |
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(Cerebral Blood Flow) Flow to thebrain matches the metabolic needs of the brain |
-Cerebralperfusion pressure(CPP): pressure needed to perfuse brain cells -Cerebral bloodvolume: amount ofblood in the cranial vault -Cerebraloxygenation: measured byO2 saturation in internal jugular vein |
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Alterations incerebral blood flow |
-Inadequatecerebral perfusion -Normalcerebral perfusion with elevated intracranial pressure -Excessivecerebral blood flow |
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CPP required after brain injury |
>70 mmHgwhile intracranial pressure is usually 1-15 mmHg |
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Increased Intracranial Pressure |
-Occurs with anincrease in intracranial content -Tumor, edema,excessive CSF, hemorrhage -Reduction involume must occur to maintain balance (lower pressure) -Firstdisplaced is CSF -If furtherreduction is needed, then cerebral blood volume is reduced -Autoregulation -Change inintracranial blood vessel diameter to maintain a constant blood flow |
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Increased intracranial pressure has how many stages? |
4 Stages |
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Stage 1 |
-Vasoconstrictionof the cerebral venous system; may be able to compensate for the pressure -Few symptoms may be seen |
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Stage 2 |
-ICP may exceedbrain’s ability to compensate via vasoconstriction -Oxygenation toneurons is compromised -Systemicarterial vasoconstriction attempts to elevate SBP to overcome IIP -Symptoms aretransient: confusion, restlessness, drowsiness, slight pupillary and breathing changes |
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Stage 3 |
-Intracranialpressure approaches arterial pressure, cerebral perfusion drops dramatically with loss of autoregulation: hypoxia and hypercapnia -Rapiddeterioration with decreased LOC, widened pulse pressure, bradycardia and small sluggish pupils |
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Stage 4 |
-Brain tissueshifts and the compartment of highest pressure herniates -Unevendistribution of pressure -Herniated area suffers further ischemia and hypoxia |
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Structural Abnormalities: Hydrocephalus |
-Imbalance ofcerebral spinal fluid, causing increased pressure in the brain -If production> absorption, CSF accumulates and pressure builds up OR -Obstruction offlow of CSF out of ventricles causes increased pressure |
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Diagnosis (Hydrocephalus) |
-May be physically apparent at birth, as in the picture -High suspicion: head circumference that crosses one ormore percentiles within a period of 2-4 wks -Frequent monitoring of head circumference (home/office), CT, MRI |
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Treatment (Hydrocephalus) |
Surgery viaNeurology/Neurosurgery |
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Care Issues(Hydrocephalus) |
-Enhance psychomotor development -Large head causes difficulties with milestones -Monitor forshunt infection/malfunction -Ventriculitis, sepsis -Increased ICP |
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Normal-Pressure Hydrocephalus |
-More common inadults -Dilation ofthe ventricles without increased pressure -Symptomshappen very slowly, mostly with memory and cognitive function -Triad ofsymptoms -Unsteady,broad-based gait with a history of falling -Incontinence -Dementia |
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Alterations in Neuromotor Function |
-Occur if thereis dysfunction in 1. Cerebral cortex 2. Pyramidal system -Axonstraveling from the brain to the spinal cord -Controlopposite sides of the body 3. Extrapyramidal system -Efferentpathways outside the medulla oblongata 4. Motor units -Normal muscletone -Slightresistance to passive motion |
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Hypotonia (muscle Tone) |
-Passivemovement with little or no resistance -Pure pyramidaltract injury (rare) -Cerebellardamage -Ataxia -Intensiontremor -Minimalweakness -Slightlyexaggerated reflexes -Weak,difficulty rising from sitting, walking up/down stairs |
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Hypertonia (muscle tone) |
-Passivemovement with resistance -Passive andactive movement is affected equally -Accidents withwalking and self-care often occur -Patients tireeasily -Musclesatrophy with decreased use, but overstimulation can cause hypertrophy| |
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Alterations in Muscle Movement |
Dysfunctionsin CNS alter muscle innervation Dopamine alsohas affects on muscle movement Paresis Paralysis |
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Dysfunctions in CNS alter muscle innervation |
Notnecessarily associated with mass or strength -Does not haveadequate strength of +5 |
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Dopamine also has affects on muscle movement |
-Too little:akinesias -Too much:chorea, tardive dyskinesia |
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Paresis |
Weakness,partial paralysis with partial loss of muscle power |
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Paralysis |
Loss of motorfunction; inability to overcome gravity |
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upper motor neuron paresis/paralysis |
-Motordysfunction in the pyramidal system -Injury canoccur in Cerebral cortex, Subcortical white matter, Brainstem, Spinal cord -Muscle overactivity, spasms, clonus |
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Spinal Shock |
-Completecessation of function below the lesion -Completeflaccid paralysis -Absence ofreflexes -Disturbance inbowel/bladder -Gradual returnof spinal reflexes after a few days/weeks -Reflexesbecome hyperactive with increase muscle tone |
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Lower Motor Neuron Syndrom |
-Involves largemotor neuron in the anterior/ventral horn of the spinal cord, motor nuclei ofthe brain stem -Voluntary andinvoluntary movement is affected -Degree ofparesis/paralysis is proportional to the number of lower motor neurons affected -Muscle hasreduced/absent tone poor/loss of reflex -Atrophies overtime -May show fasciculations -Amyotrophies originate inthe anterior horncells or motor nuclei of the Cranial Nerves -Musclestrength, tone and bulk are affected |
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Poliomyelitis |
-Severeinflammation or motor neurons from polio virus -Some may dieand lead to paralysis |
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Guillain-BarreSyndrome |
-Affectedanterior horn and motor nuclei of CN extend proximally to cause impairmentto the nerve roots and motor neurons -If enough aredestroyed, permanent motor loss results (cannot regenerate without the cellbody) -ProgressiveSpinal Muscular Atrophy -Anterior horncells are involved and muscle weakness>>paralysis |
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Bulbar Palsy |
-Involves theCNs from the bulb: CN IX, X, XII -Paresis/paralysisof jaw, face, pharynx, and tongue |
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Hyperkinesia |
excessivemuscle movements |
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Dyskinesia |
"abnormalinvoluntary movements" -TardiveDyskinesia -Movement ofthe face, trunk and extremities -Mostcharacteristic is continual chewing with lip smacking -Often as aSide Effect of phenothiazines |
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Huntington Disease(Hyperkinesia) |
-Rare,hereditary disease involving the basal ganglia and cerebral cortex (3-7 per100,000) -Degenerative,hyperkinetic movement disorder -Onset isusually after it has been passed on to the offspring (25-45 yr) |
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(Huntington Disease) Pathologic feature is abnormal movement |
-Severedegeneration of the basal ganglia (triggers are unknown) -Basal ganglia:important for connections with other parts of the brain -Tangles ofHuntington protein contribute to neuronal loss -Biochemicalalteration is the depletion of GABA (inhibitory neurotransmitter) -Results inpoor integration of motor and mental function -Frontalcerebral atrophy occurs later in the disease -Voluntaryskeletal movement, fine repetitive motion, eye movement |
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Clinical, Progression, Treatment of Huntington |
-Clinical picture is mostly movement issues initially -Involuntary,fragmentary movement progresses to excessive movement (chorea) -Starts at faceand hands and involves the whole body -Progressivedecline in intellect and thought processes (dementia) -Slowedthinking, cognitive deficitsn -No currenteffective treatment to halt the process, but some medications are being explored |
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Abnormal Movements Hypokinesia |
Loss ofvoluntary movement even though consciousness is preserved, along with normalperipheral nerve and muscle function |
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Akinesia |
-Decrease involuntary movements -Defect inextrapyramidal system, involving dopamine |
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Bradykinesia |
-Slowness ofvoluntary movements with difficulty -Initiatingmovement -Continuingmovement smoothly -Performingtasks at the same time or one after the other |
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Loss of associated movement |
Expressionlessface, statue posture, no speech inflection, spontaneous gestures |
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Parkinson Disease (hypokinesia) |
Commondisorder of movement (1 in 272) |
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SecondaryParkinson Disease |
-Caused by adisorder other than Parkinson -Head trauma,infection, neoplasm, toxins, drug intoxication -Drug-inducedis usually reversible |
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PrimaryParkinson disease |
-More prevalentin the elderly (>60 yrs) and males -Pathogenesisunknown, but possibly gene, viral, and/or environmental toxin -Degenerationof basal ganglia and loss of dopamine-producing neurons (inhibitory) -Cholinergic isin excess (excitatory) and results in hypertonia (tremors/rigidity) |
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Clinical, Progression, Evaluation, Treatment Parkinson Disease |
-Clinicalpicture is one of abnormal movement (insidious) -Akinesia/bradykinesia,muscle stiffness (difficulty walking) -Restingtremors -Disorderedequilibrium due to inability to make postural changes -Dysarthria anddysphagia (slurred speech, drooling) -Progressiveprocess and all above manifestations will occur -May startunilateral but will become bilateral -Progressivedementia occurs, but generally over 70 years old -Evaluation:exclude causes for secondary Parkinson/ PET scan -Treatment -Medicationsdecrease akinesia, but MANY side effects (mental status) so often not startedin early stages |
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Disorder of Stance DecorticatePosturing |
-Brainstem isnot inhibited by the cerebral cortex motor area -Flexed at theelbows and close to body -LE extended |
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Disorder of Stance Decerebrate Posturing |
-Severe injuryto brain and brain stem -Overstimulationof postural righting and vestibular reflexes -Increased tonein extensor muscles |
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Disorders of Expression |
All involvethe motor aspect of communication |
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Hypermimesis |
Pathologiclaughter(right hemisphere)or crying (left hemisphere) |
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Hypomimesis |
-Loss ofemotional language (right hemisphere damage) -Expressive:inability to express emotion via speech or facial expression -Receptive:inability to understand emotion or facial expression |
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Dyspraxia/apraxia |
-Occurs when Land R cerebral cortex pathways are interrupted -Gray matter(cell bodies) cannot communicate effectively -Voluntarymovement needed for coordinated movements -Speaking,writing, using tools, playing sports, following instructions |
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Brain Trauma Causes |
-Transportation-related(MVA, PVC, bike, skateboard) -Falls -Sports-related -Violence |
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Brain Trauma Improved Survival Rates due to |
-Advancementsin safety measures -Reduced timeto medical care -Trauma centers -Improvedon-scene medical management |
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Brain trauma injury can be |
-Closed blunttrauma (more common) -Dura intact/noexposure of brain to the environment -Openpenetrating trauma -Break in thedura /cranial contents is exposed to the environment |
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Mechanisms of Brain Injury |
Primary Secondary Tertiary (days or months later) |
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Primary |
Caused byimpact: neural injury and vascular responses |
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Secondary |
-Indirectconsequence of the injury, causing further neuronal injury or death -Alteredcerebral blood flow, hypoxia, ischemia, inflammation, edema, IICP, herniation |
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Tertiary |
-Consequence ofprimary and secondary injury and systemic complications that contribute to further brain injury -Pneumonia,fever, infections, immobility |
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Brain Trauma Focal Injury |
-Affecting onearea of the brain -50% of allbrain trauma but 67% of head injury deaths -Very preciselocation, occurring from a contusion that can cause epidural, subdural andintracerebral hemorrhages -Smaller areaof impact, the greater the severity of injury |
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Brain Trauma Diffuse Axonal Injury |
-Involving morethan one area of the brain -50% of allbrain trauma with 33% of brain injury deaths -More disabledsurvivors2 |
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Focal Brain Injury |
-Lesion occursin a precise location, causing a contusion -Blood leaksfrom the vessel resulting in a hematoma or hemorrhage -Injury isusually coup-contrecoup motion -The smallerthe area of impact, the more severe the injury -Brain edemaaround injured tissue -Increased ICP -Peak affect is18-36 hours -Frontal lobeis most common -Attention,memory and executive function -May have lossof -Consciousness(<5 min) -Reflexes(falls to the ground) -Respirations(transient cessation) -Normal HR(brief period of bradycardia) -Blood pressureregulation (decreased BP) |
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Clincal, Progression, Evaluation, Treatment of Focal Brain Injury |
-Soon after theinjury VS stabilize to normal and reflexes return -Consciousnessis regained -Residualdeficits may remain, pending the severity of the impact -Some neverregain preinjury LOC -Evaluation -History andphysical -Testing fordetails of injury severity -Xrays, computedtomography (CT), magnetic resonance imaging (MRI) -Treatment -Hemorrhagesmay need evacuation -Care is aimedat controlling ICP and symptoms |
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Brain Hematomas |
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Penetrating Brain Trauma |
-Compoundfracture -Opencommunication between brain and environment -Bone fragmentcan cause direct injury -Cranial nervescan be injured with a basilar skull fracture -Missileinjuries: bullets, rocks, knives, shell fragments -Crush orstretch injury -Clinicalpicture -Most loseconsciousness with coma dependent severity of injury -Major issues -Remove debris,blood clots and clean the area (antibiotics) -Manage ICP |
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Diffuse Brain Injury |
-Also calledDiffuse Axonal Injury (DAI) -Widespreaddamage to axonal fibers and white matter -Severitycorrelates with amount of shearing force -Reduces speedof informational processing and disrupts attention span -Most severeinjury is located more peripheral to the brain stem -Extensivecognitive and affective impairment -Damagecontinues 12 hrs to daysafterwards -Injury cancause acute brain swelling from -Increasedintravascular flow within the brain -Vasodilation -Increasedcerebral blood volume |
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Categories of DAI |
Mildconcussion Classiccerebral concussion Mild diffuseaxonal injury Moderatediffuse axonal injury Severe diffuseaxonal injury |
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Mildconcussion |
-No LOC, butconfused for several minutes -Possibleretrograde amnesia, headache and not “being themselves” for days |
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Classiccerebral concussion |
-Up to 6 hrs LOC with lossof reflexes and decreased RR, HR and BP but stabilizes quickly -Bothretrograde and anterograde amnesia along with confusion for hrs to days -Inability toconcentrate, fatigue, headache, forgetfulness, irritability, insomnia, moodswings |
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Mild diffuseaxonal injury |
Decerebrate ordecorticate posturing in 30% with prolonged stupor |
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Moderatediffuse axonal injury |
-GCS of 4-8with improvement to 6-8 by 24 hrs, with LOC for days/weeks -When awakens,confused with anterograde and retrograde amnesia for extended time -Permanentchanges in memory, attention, executive functions, reasoning, vision, language |
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Severe diffuseaxonal injury |
Outcome morebleak: severely compromised skills, inability to learn, behavior problems |
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Secondary Brain Injury |
-Indirectresult of primary brain trauma -Due tointracranial processes and hypermetabolic state resulting in -Cerebral edema -Increased ICP -Decreasedcerebral perfusion pressure -Ischemia -Brainherniation -Management isrelated to preventing complications and managing actual problems -Removal ofhematoma, management of hypotension hypoxemia ICP, fluid replacement,temperature and respirations |
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Spinal Cord Trauma |
-Occurs -Due to motorvehicle accidents, falls, violence and sports -Fromacceleration, deceleration, or deformation forces -At the mostmobile spinal areas: C1 to C2, C4 to C7, T10 to L2 |
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4 Classification of Spinal Cord Injuries |
SimpleFracture spinous process Compressed Vertebral Fracture Comminuted(burst) fracture Dislocation |
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Spinal Cord Trauma Cont. |
-Gray and whitematter are both damaged -Severely atthe level of injury plus 2 segments above and below -Tissuenecrosis may occur when oxygen is decreased -Cord swellingalso increases dysfunction -White matterreturns to normal before the gray matter |
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Spinal Shock |
-Reflexfunction below the lesion is lost -Skeletalmuscles -Bowel/bladder/sexualfunction -Autonomiccontrol -Lasts days to3 months -Reflexes,spasticity and hyperreflexia begin to reappear |
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permanent transection vs partial transection |
-Permanent lossof motor and sensory function are lost with complete transection (quadriplegia/paraplesia) -Partialtransection has variable losses, pending severity and level of injury -Anterior horn(ventral root): efferent, loss of movement -Posterior horn(dorsal root): afferent, loss of sensation |
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Major Dermatomes to know |
-C3: neck -C6: radialside of arm -C8: ring andsmall finger -T4: nipples -L1: inguinal -L4: knee -L5: shin,ankle, foot -S5: anal area |
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Autonomic Hyperreflexia |
-Life-threateningcondition that occurs after spinal shock resolves, most commonly for injuries T6 or above -SANSstimulation occurs and results in massive, uncompensated cardiovascular event -Hypertension(up to 300mmHg systolic) and bradycardia -Headache,blurred vision -Sweating above thelesion level -Nausea -Caused bystimulation of sensory receptors below the level of the lesion -Example:Distended bladder/rectum -Requires promptemptying |
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Degenerativedisc disease |
-Disk can herniate and pinch the spinal nerve -Most have nofunctional incapacity due to pain |
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Spondylosis |
Defect in thelamina or neural arch of vertebra |
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Spondylolisthesis |
Vertebraslides forward onto the vertebra below |
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Spinalstenosis |
Narrowing ofthe spinal canal |
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Cerebrovascular Disorders |
-Brainabnormality due to pathologic process in the blood vessels -Ischemia withor without infarction -Hemorrhage -CerebralVascular Accident (CVA) -Also commonlyknown as a stroke -Leading causeof disability -More common in the elderly, blacks 2X greater than whites -Increased riskwith -Hypertension -Type 2Diabetes -Smoking -Polycythemia -Impairedcardiac function |
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Thrombotic CVA (cerebral thrombosis) |
-Occlusion ofarteries supplying brain due to thrombi -Thrombosisdevelops from atherosclerosis and inflammatory disease -Ulcered area of thevessel has platelets/fibrin adhere for repair, but may instead cause a clot andocclude the vessel -May occur as aTransient Ischemic Attack (TIA) -Likely due toplatelet clumps or vessel narrowing which causes intermittent blockage -Neurologicdysfunction lasts no more than 1 hourwith complete recovery -Focalneurologic signs are seen |
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Neurological Assessment: Focal Neurologic Sign |
-Impairments ofnerve, spinal cord, or brain functionthat affects a specific region of the body -Examples -weakness inthe left arm -paresis or plegia -The finding offocal signs indicates aneed for a fullneurologic exam -Concussion -Trauma |
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Focal Signs- Frontal Lobe |
Gait, musclemovement, seizures |
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Focal Signs- Parietal Lobe |
Sensation andproprioception |
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Focal Signs- Temporal Lobe |
Auditory,hallucinations, partial seizures and memory |
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Focal Signs- Occipital |
Visual:blindness, agnosias, and visualhallucinations |
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Focal Signs- Limbic |
Memory anddecision-making skills |
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Focal Signs-Cerebellar |
Balance andcoordination |
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Focal Signs-Brainstem |
Variedsensory-motor issues and CNS |
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Focal Signs- Spinal Cord |
unilateralparalysis with contralateral loss of pain sensation |
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Embolic CVA |
-Thrombusfragments come from outside the brain -Obstructssmall brain vessels causing ischemia -Risk factors -Atrialfibrillation -Leftventricular aneurism or thrombus -Left atrialthrombus -Recent MI -Endocarditisor rheumatic valve disease -Mechanicalheart valves -Second strokeusually follows because the source is still present |
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Hemorrhagic CVA (bleeding) |
-Intracranialhemorrhage occurs mostly from hypertension -Rupturedaneurysm, vascular malformation, bleeding into a tumor, hemorrhage from anticoagulants, head trauma, illicit drug use -Blood forms amass and compresses adjacent brain tissue -May seep intothe ventricular system -Common sites -Basal ganglia -Thalamus -Cortex -Pons -cerebellum |
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Thrombotic vs Embolic vs Cerebral Hemorrage |
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Intracranial Aneurism |
-Abnormality inthe vasculature -Rupture occursin the thin area -Hemorrhagingblood into the brain -Severitydepends on location and amount of bleeding -Can causebrain death -Bleedingcauses pressure to the brain -Ceasesbleeding when fibrin-platelet plug forms -Blood isreabsorbed over a few weeks -Most commonneurological signs are cranial nerves: III, IV, V & VI -Oncediagnosed, treatment is dependent on clinical status -Surgery,endovascular coil embolization, or symptom management |
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Vascular Malformation |
-Arteriovenousmalformation (AVM) -Mass ofvessels creating abnormal channels between arterial and venous systems -Usuallypresent at birth, but often not exhibited until ~20’s and up -A bruit may beheard if in the carotid or mastoid process -Clinicalpresentation -Chronicnondescript headache (25%) -Seizure (50%) -Intracerebral,subarachnoid, or subdural hematoma (50%) -Can resemblestroke or ruptured aneurism -Must beconfirmed by MRI and CT and possibly MRA |
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Subarachnoid Hemorrhage |
-Commonly seenwith intracranial aneurisms, AVM, andhypertension -Subarachnoidspace fills with blood -Increasesintracranial volume (IICP) -Irritatesneural tissue -Impairs CSFreabsorption and circulation -Resulting inmore volume -Mortality is50% at 1 month |
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Clinical and Treatment Hemorrhage |
-Clinicalpicture -Headaches ,changes in LOC, vomiting, focal neurologic signs -If bleed isexcessive, symptoms are faster and more severe -visualdisturbances -motor deficits -loss ofconsciousness -Meningealirritation causes nuchal rigidity (+ Kernig/Bradzinski) -Re-bleedingcan occur after 1st bleed, greatest within 2 weeks -Treatment -Correct theunderlying aneurism or AVM -ControllingICP, improve perfusion, prevent ischemia |
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Assessment of Meningeal Signs: Kernig |
-Irritation ofmotor nerve roots passing through inflamed meninges as the roots are broughtunder tension and produce pain -Kernig -Usuallyperformed with the patient supine withhip and knee in flexion -Extension ofthe knees is attempted -The inabilityto extend the patient’s knees beyond 135degrees without causing pain constitutesa positive test - |
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Assessment of Meningeal Signs Brudzinski: Standard Reflex Sign |
-Patientsupine, place one hand behind the patient’s head and the other on the patient’s chest -Raise thepatient’s head while the hand on the chest prevents the patient from rising -Flexion ofthe patient’s lower extremities (hips and knees) constitutes a positive sign -Brudzinski’s neck sign hasmore sensitivity than Kernig’s sign |
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Infections in the CNS |
-Bacteria,viruses, fungi, parasites and mycobacteria -Enters the CNSvia -Bloodstream(gets through the BBB) -Directlyinvading from penetrating wound -Inflammatoryresponse can cause edema and harm (IICP) -Commondiseases include -Meningitis -Encephalitis |
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Meningitis |
-Inflammationof the brain and spinal cord -Significant cause ofillness in pediatrics -Infection of the cerebral meninges -Bacterial agents -group B streptococci -E. coli, Listeria -Hemophilus influenza and Streptococcus pneumoniae -Less prevalent since Haemophilus influenza type B (Hib) andpneumococcus immunizations -Neisseria meningitides (meningococcal meningitis) -only form that is transmitted to others -Viral Agents -Measles, mumps, herpes, enteroviruses |
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Bacterial Meningitis |
•Routeof infection is by vascular dissemination from a focus of infection elsewhere,such as a URI (“Murphy’s law”) •EXCEPTNeisseriameningitides:droplet infection from Nasopharyngeal secretions •Alsovia penetrating wounds, skull fractures, Lumbar Puncture (poor technique), infectedVentroperitoneal shunt] |
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Bacterial Meningitis < 2 years |
•Fever,Lethargy, irritability •Vomiting •Bulging fontanel,seizures •High pitched cry •Stiff neck –late sign or not seen, especially in the under 12 month group |
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Bacterial Meningitis > 2 years |
•Fever,lethargy •Headache •Vomiting •Seizures –late sign •Nuchalrigidity •+ Kernig and Brudzinski |
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Serious Complications |
•Meningococcemia(Neisseriameningitides) •Predominantlyschool-age children and adolescents •Purpura commonlyseen and is a medical emergency •Verycontagious (droplet organism) •Severe onsetwith rapid deterioration •Develops intooverwhelming septic shock •DIC •Massivebilateral adrenal hemorrhage •Purpura •Treatment mustbe immediate •High mortality |
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Aseptic Meningitis |
•Causes •Virus:measles, mumps, herpes, enteroviruses •Leukemia •Onset isabrupt or gradual •Similarclinical findings but generally mild •Self-limitingdisease •Treatment issymptomatic and supportive |
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Meningitis: Evaluation and Treatment |
•Firstdetermine the cause: viral versus bacterial •Blood cultures •CBC with differential, UA, andchemistry panel •Lumbarpuncture •Increased WBCsare seen inboth •MononuclearWBCs in viral (monocytes) •also, noinfectious agent is found •Polymorphonuclear WBCs inbacterial (neutrophils) •Nose andthroat cultures if CSF test is negative tolook for offending agent •EEG, CT or MRI(even brain biopsy may be needed) •Treatment •Antibioticsfor bacterial, supportive care for viral •Familyteaching •Care during the infectious stage •Possible sequela: Hearing/vision loss, recurrent seizures, cognitive and motor impairments |
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Encephalitis |
•Acute febrileillness that involves the nervous system •Usually viral •Spread by mosquito (West Nile Virus) •Herpes simplex type 1 •Complication of current systemic viral disease (poliomyelitis, mononucleosis) •After recovery from a viral infection (rubella or rubeola) •Involves themeninges and can cause nerve cell degeneration •Edema,necrosis and IICP •Clinical picture •Mild to life-threatening •Fever,delirium, progressive confusion, seizure, CN palsies, paresis/paralysis, IICP •Most are self limiting, but can cause permanent damage |
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Demyelinating Disorders |
•Damage to themyelin sheath in the axon affects neural transmission •MultipleSclerosis •Relativelycommon: •Begins ages20-40 years •AmyotrophicLateral Sclerosis •AKA, LouGehrig disease •Less commonand 10% are genetically linked •Begins after40 years, peaks in 50’s |
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Multiple Sclerosis |
•Autoimmunedisorder, triggered in a susceptible person •Inflammationcontributes to the demyelination •Activatedimmune cells produce a toxin •Focal changesbut also diffuse throughout the CNS •MSlesions occur in gray or white matter creating plaques (sclerosis) •Can alsochange constituents of myelin and causeatrophy of brain •Clinicalpicture •Initialsymptoms include face, trunk, limbs (paresthesia and weakness) •Visualdisturbances, urinary incontinence, cognitive changes, emotional lability •Diseaseprocess is variable •Remitting-relapsing(90% present like this) •Primaryprogressive •Progressiverelapsing |
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Multiple Sclerosis- Clinical Path and Treatment |
•Clinical Path •Pending thetreatment, how soon it is initiated, and type of course •Often haveshort-lived attacks •Increase inserum calcium or body temperature (increases leakage through delyelinated area) •Functionaldemands exceeding conduction capacity •Advanced MShas cerebellar symptoms: slurred speech, ataxia and intention tremor •Diagnosis andTreatment •MRI is mostsensitive to identify the lesions •Goal is toprevent exacerbations and permanent neurologic damage •Drugs for thedisease are immunosuppressive •Research isshowing that Vit D may prevent disease progression •Other drugsare to control symptoms •Teaching:exercise but no extreme fatigue, stop smoking, avoid heat exposure |
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Amyotrophic Lateral Sclerosis |
•Diffuselyinvolves both upper and lower motor neurons •Progressivemuscle weakness, culminating in inability to breathe •Cause of motorneuron death is unknown •Neuronsdegenerate, but no inflammation is present •Demyelinationoccurs and scarring forms, causing sclerosis •Can begin ineither the upper or lower motor neurons, or both •Clinicalpicture •Muscleweakness usually begins in legs/arms leading to atrophy •Loss ofdexterity, inability to walk, speak, swallow, and finally, breathe •Death withinabout 2-5 years, pending care •Mentallyintact! •Diagnosis andTreatment •EMG, musclebiopsy, CSF biomarkers, scans (ruling out other causes) •No realmedications to alter the course of the disease •Support forfamily and patient—DNR status? Palliative care? |
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Myasthenia Gravis |
•Neuromusculardisorder •Acquiredautoimmune disease •Body sees thepostsynaptic receptors as “foreign” and produces antibodies • Antibodiesfix on the Acetylcholine receptor at the neuromuscular junction •Nerve impulsetransmission is impaired, resulting in weakness and fatigue •Over time, theantibodies destroy the receptor sites •Muscle cellscannot receive transmissions and action is halted |
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Myasthenia Gravis Clinical Picture |
•Clinicalpicture •Insidiousonset with general complaints of muscle fatigue and weakness •Muscles of theeyes, face, mouth, throat, neck are first affected •Progressesover time to include the diaphragm>>impaired ventilation •Myasthenic crisis:severe bout of weakness causing paresis/paralysis •Cholinergiccrisis: ^intestinal motility and cramps, diarrhea, bradycardia, pupillary constriction diaphoresis |
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Myasthenia Gravis Diagnosis and Treatment |
•Diagnosis •Tensilon isadministered and the patient improves tremendously for a few minutes •EMG, detectionof Acetylcholine antibodies •Treatment •Disease hasremissions/exacerbations over time •May needventilator support •Drugs include •Anticholinesterasedrugs , steroids, immunosuppressant drugs •ForCholinergic crisis, anticholinergic drugs are held til nontoxic •Thymectomy: terminatesthe production of self-reactive T cells and B cells that produce antibodies |
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Cranial Tumors |
•Can be primaryor metastatic •20-40% ofcancer patients with metastasis will have it in the brain •Damage occursin two mechanisms •Destructiveaction of the tumor itself •Compressionfrom tumor causing decreased blood flow to the brain •Primary tumor •Originates inthe brain and does not generally metastasize (no lymph) •Treatment •Surgicalexcision or decompression •Chemotherapy •Radiotherapy •Hyperthermia •Goal is toreduce edema, this preventing IICP |
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Neurofibromatosis Tumor suppressing protein is missing (genetic) Genetic testing is available (prenatal) TYPE 1 |
•peripheralneurofibromatosis •More common (1in 3500) •Multiplecutaneous lesions •Café-au lait spots •Less commonbone and soft tissue tumors •Learningdisabilities in 50%: |
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Neurofibromatosis Tumor suppressing protein is missing (genetic)Genetic testing is available (prenatal) TYPE 2 |
•Central neurofibromatosis •Rare (1 per60,000) •Centralnervous system tumors •Vestibularnerves often affected •Hearing loss,deafness, balance issues •Optic nervetumors •Loss of visualacuity |
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Spinal Cord Tumors |
•Rare, and only2% of all CNS tumors •Can originate •Within theneural tissue (intramedullary) •Primarilygliomas and difficult to surgically remove completely •Damages cordby invading the cord and also pressure/compression •From tissuesoutside the spinal cord \ (extramedullary) •Usually eitherneurofibromas or meningiomas and can beremoved completely •If not, itwill compress tissues, including the cord •Capable ofmetastasis from seeding in CSF andbloodstream |