Class 6: Neurological Flashcards
Primary motor area
-Precenteral gyrus; motor control & movement on the opposite side of the body
Supplemental motor area
-Anterior to precenteral gyrus; proximal muscle activity, stance, gait, spontaneous movement & coordination
Somatic sensory area
Postcentral gyrus; process sensory response from opposite side of the body
Association sensory areas (PAPA)
-Parietal lobe; integrates somatic & sensory inputs
-Posterior temporal lobe; integrates visual & auditory language comprehension
-Anterior temporal lobe; integrates past experiences
-Anterior frontal lobe; controls higher-order processes
Basal ganglia
-Near lateral ventricles of both hemispheres; control & facilitate autonomic movements
Thalamus
-Below basal ganglia
-Relays sensory & motor inputs to the cortex
Hypothalamus
Regulates endocrine & autonomic functions
Limbic system
-Lateral to hypothalamus
-Influences affective behaviour & basic drives (feeding & sexual behaviour)
Slide 8
LOC + disorientation
Beginning loss of consciousness; first to time then place, then memory and finally to self recognition
LOC + lethargy
Limited spontaneous movement or speech; easy arousal with normal speech or touch; possibly a&o x3
LOC + obtundation
Mild to moderate reduction in arousal with limited response to environment, falls asleep unless stimulated, answers questions with minimal response
LOC + Stupor
Condition of deep sleep or unresponsiveness unless vigorous & repeated stimulation; response is often withdrawal or grabbing at stimulus (withdrawal better than grabbing)
LOC + Coma
No verbal response to any stimuli; noxious stimuli such as deep pain or suctioning do not yield movement
LOC + Light coma
Associated with purposeful movement on stimulation
LOC + coma
Associated with nonpurposeful movement only on stimulation
LOC + Deep coma
Associated with unresponsiveness or no response to any stimuli
Neurological assessment
-GCS
-NIH stroke scale
-Orientation/NVS
-Spinal signs
-Pupils & LOC always
Neuro assessment steps
- NOD, assess A&O x3 (skip to 2 if unconscious)
- Vitals
- NVS
NVS
-Eye opening (spontaneous, to speech, to pain or none)
-Best verbal response (A&O x3, confused? Innapropriate words, incomprehensible sounds, none)
-Best motor response (obeys command, localizes pain, flexion withdrawal, flexion abnormal, extension abnormal, none)
Slide 18 & 19
Pupillary response + metabolic imbalance
Small, reactive & regular
Pupillary response in dysfunction of tectum (roof) of the midbrain
Large “fixed” hippus
Pupillary response + pontine dysfunction
Pinpoint
Pupillary response + midbrain dysfunction
Midposition and fixed
Pupillary response + dysfunction of third cranial nerve
Sluggish, dilated, and fixed
Pupillary response + diencephalic dysfunction
Small & reactive
Abnormal posturing
Abnormal response to pain, limb goes into extension
Abnormal motor responses with decreased responsiveness (decorticate & decerebrate)
-Decorticate; hemispheric damage above the midbrain releasing medullary and pontine reticulospinal systems
-Decerebrate; opisthotonos (associated with severe damage involving midbrain or upper pons), acute brain injury (causes limb extension regardless of location)
Abnormal motor responses with decreased responsiveness (others)
-Extensor responses in upper extremities accompanied by flexion in lower extremities; pons
-Flaccid state with little or no motor response to stimuli; lower pons & upper medulla
Slide 22, is decerebrate or decorticate worse?
-Note plantar flexion in both
-Decerebrate is worse
NVS/CNS
-LOC (GCS), PERRLA, lightheadedness, dizzy
-Pain, sedation/analgesic/sleep
-ICP, external ventricular drain, cerebrospinal drainage, C-spine traction/braces
-Halo sign, otorrhea & battle sign
Apneusis
-Prolonged inspiratory cramp (pause at full inspiration); common variant is a brief end-inspiratory pause of 2 or 3 seconds often alternating with an end-expiratory pause
-Damage to respiratory control mechanism at the pontine level; pontine infarction but documented with hypoglycemia, anoxia & meningitis
Central neurogenic hyperventilation
-Sustained deep, rapid, but regular pattern (hyperpnea) occurs, with a decreased PaCO2 and a corresponding increase in pH & PO2
-Result of CNS damage or disease involving the midbrain & upper pons; seen after IICP and blunt head trauma
Cheyne-stokes respirations
Smooth increasing breathing pattern (crescendo) in rate and depth of breathing (hyperpnea), which peaks and is followed by a gradual smooth decrease (decrescendo) in rate and depth of breathing to the point of apnea. The hyperpneic phase lasts longer than the apneic phase
Cheyne-stoke respirations location of injury
Bilateral dysfunction of deep cerebral or diencephalic structures; seen with supraentorial injury and metabolically induced coma states
Cluster breathing
-Cluster of breaths with irregular pauses between breaths
-Dyfunction in lower pontine and high medullary areas
Ataxic breathing
-Irregular breathing occurs, random shallow & deep breaths and irregular pauses, rate is often slow
-Primary dysfunction of medullary neurons that control breathing
-Reticular formation of the medulla
Abnormal oculomotor responses
-Slide 27
-Dolls eyes
-Cold water test; brain dead pt will not respond
-Eyes move with the head and do not deviate
Mechanisms in the lower brainstem
-Hiccuping, vomiting and yawning are r/t the medulla
-Projectile vomiting w/o nausea represents a compression of the medulla
-Vomiting w/o nausea indicates a neuro problem
Pain, sensation & dermatomes
-Assess from bottom up
-Slide 29
Alterations in cerebral hemodynamics
-Brain reacts to an injury through aCerebral blood flow, ICP and O2 delivery
-Changes in cerebral blood flow d/t :
-Inadequate cerebral perfusion, normal cerebral perfusion, or elevated ICP
IICP pathophysiology
-If the pressure is able to be displaced to a cranial vault, the pressure is unchanged
-If the pressure is unable to be displaced to another area then IICP
Etiology of IICP
-Increased in intracranial content; tumor
-Edema, excess CSF
-Intracranial hematomas or Hemorrhage
-Metabolic and physiological factors; C02, 02, fever, pain
-Vascular anomalies; Arteriovenous malformations (spider web; cluster of thin walled arteries & vein, increased risk for hemorrhage)
Increased breathing + IICP
-Increased breathing increases ICP
Fever + IICP
Fever increases metabolic rate resulting in an IICP
Nursing management of IICP
Head of bed at 30 degrees, lights low, calm
Progression of IICP: Stage 1
-Stage 1: Intracranial HTN; little change in ICP, no manifestations except through ICP monitoring, vasoconstriction and external compression of the venous system compensates
Progression of IICP: Stage 2
-Intracranial HTN; IICP, O2 changes, systemic arterial vasoconstriction occurs to elevate the systemic BP to overcome IICP
-Manifestations: Confusion, restless, drowsy, aPupillary & breathing
Progression of IICP: Stage 3
-Intracranial HTN; hypoxia & hypercapnia, dramatic changes to condition, cushing’s triad presents
-Manifestations; aArousal or central neurogenic hyperventilation, widened pulse pressure, bradycardia, small sluggish pupils
Progression of IICP: Stage 4
-Intracranial HTN; brain shifts & herniates, compromised blood supply causing ischemia & hypoxia, increased pressure leads to small hemorrhages, obstructive hydrocephalus
IICP priority assessments
LOC & pupillary changes
Pressure on ocular nerve
aVision, dizzy, affects RAS
Cerebral edema types
Vasogenic cerebral edema; caused by increased permeability of the capillary endothelium
Cytotoxic cerebral edema; increment in total brain water produced, cells swell
Interstitial cerebral edema
IICP manifestations
-aLOC & VS
-Cushing’s Triad (widening pulse pressure, bradycardia, irregular respirations
-Ocular signs
-Decreased motor function; abnormal posturing
-Headache, vomiting
Nursing assessment of IICP
-Pupils, VS, gait, movement, posturing & headache
Early signs of IICP
-Compensatory mechanisms intact
-aLOC, unilateral pupil change in PERRLA
-aResp
-Unilateral hemiparesis
Early variable signs of IICP
-Focal findings (aSpeech & vision)
-Papilledema
-Vomiting, headache & seizures
Late signs of IICP
-Compensatory mechanisms failing
-Decreased LOC
-Unilateral/bilateral PERRLA
-Ineffective breathing (cheyne-stokes)
-aMotor response (decorticate or decerebrate)
Late/terminal variable signs of IICP
-HTN with widened pulse pressure
-Bradycardia
-Hyperthermia
Terminal signs of IICP
-Coma
-Bilateral fixed & dilated pupils
-Respiratory arrest
-Absence of motor response (flaccid)
At 41 degrees
More prone to seizures
At 43 degrees
w/o correction will lead to death
IICP assessment (neuro)
-aLOC, monitor for deterioration to worst case
-Coma & unresponsive
-Pupillary changes unilaterally & bilaterally, equal, abnormal in shape, size, reactivity
-Does the patient follow commands, MP weak/strong, equal upper/lower; abnormal posturing, flaccid
-Headache, aVision
IICP assessment (CV)
-Bradycardia, widening pulse pressure (sign of Cushing’s triad), HTN
-Are there any changes in perfusion, cap refill, pulses
IICP assessment (resp)
-Monitor for changes in respirations: Bradypnea, tachypnea, irregular, Cheyne’s stoke present or absent
IICP assessment (renal)
-Urine output, is it > or < 30 cc/hr, colour, consistency, frequency, 24 hour fluid balance
Slide 40
Traumatic brain injury
-Alteration in brain function
-Caused by an external force; falls are most common
-Classified as primary or secondary
Primary brain injury (focal brain injury) + closed
-Coup/ contrecoup, contusions
-Epidural & subdural hematomas
-Subarachnoid hemorrhage
Primary brain injury (focal brain injury) + open
-Compound fracture (diffuse axonal injury can occur with a focal injury)
Secondary brain injury
Cell death
Primary injury (focal brain injury)
-Scalp laceration, skull fracture, contusions
-Epidural subdural, intracerebral and subarachnoid hemorrhages
Diffuse (acceleration/deceleration rotation)
-Concussion
-Diffuse axonal injury: Mild to severe over widespread area
Secondary brain injuries
-Hypotension, hypoxia, cerebral ischemia, cerebral edema
-Impaired autoregulation of blood flow
-IICP, inflammation, neuronal death
-Excitotoxicity, oxidative stress
-Vascular injury and blood brain dysfunction
Traumatic brain injury definition
-Any trauma to the scalp, the skull or the brain
-High potential for a poor outcome
Types of traumatic brain injuries
-Scalp lacerations (focal/open)
-Skull fractures (focal/open):
-Linear or depressed
-Simple, comminuted or compound
-Open or closed
Comminuted skull fracture
Multiple linear fractures with bone fragmentation (direct high momentum impact)
Compound skull fracture
Depressed skull fracture and scalp laceration with communicating pathway to intracranial cavity
Diffuse brain injury
-Involves widespread areas of the brain
-Acceleration & deceleration, such as whiplash and rotation causes shearing of axonal fibers and white matter tracts
-Not immediately associated with intracranial HTN but brain swelling caused by increased blood flow, vasodilation, and increased blood volume can result in death
DAI can…
Breaks capillaries in their eyelids
Hemotomas & types
-Collection of blood
-Epidural
-Subdural: acute, subacute & chronic
-Intracerebral: Intracranial & subarachnoid
Epidural hematoma
Collection of blood from bleeding between the dura and the inner surface of the skull
Subdural hematoma
Collection of blood that results from bleeding between the dura mater and the arachnoid layer of the meningeal covering of the brain
Subdural hematoma acute stage
-Manifest within 48 hours
Subdural hematoma subacute stage
2-14 days
Chronic subdural hematoma
Develops over weeks or months after a seemingly minor head injury
In a right sided fall, look for
Right pupillary changes
Intracerebral (intracranial) hematoma
-Collection of blood within the parenchyma that results from bleeding within the brain tissue
-Occurs in the frontal and temporal lobes
-Blood cannot be evacuated
Traumatic subarachnoid hematoma
-Hemorrhage d/t traumatic forces that damage the vascular structure in the subarachnoid space
-May predispose the patient to cerebral vasospasm and diminished cerebral blood flow, increasing the risk of ischemic damage
Nursing assessment of hematomas
Monitor for signs of IICP, GCS, NVS, Kernig sign and Brudzinski sign (SAH) & airway compromise
In concussions time is most important
Mild concussion
-Loss of consciousness may last >30 min , usually caused by blunt force
-GCS= 13-15, confusional state last 1 to several minutes
-Headache, N/V, difficulty concetrating & sleeping for a few days
-May need a CT
Moderate concussion
-Loss of consciousness >30mins>6 hours
-GCS= 9-12
-Possible skull fracture, no brainstem injury
-Transitory decerebration or decorticate posturing may occur
-Amnesia may last >24 hrs
-Abnormal brain imaging
Moderate concussion problems
-Permanent deficits in selective attention, vigilance, detection, working memory, data processing, vision or perception and language, may also be mood and affect changes ranging from mild to severe
Basal skull fracture
-Fracture to the base of skull
-‘Battle sign’, bruising behind the ear
-CSF may drain from the nose (rhinorrhea) and ear (otorrhea)
-Halo sign (blood encircled with yellowish CSF)
Severe concussion
-Loss of consciousness for > 6 hrs
-GCS= 3-8
-Permanent neurological deficits
Severe concussion + learning
Inability to learn and reason, inability to modulate behavior
Severe concussion + coordination & communication
Compromised coordination and verbal and written communication
Severe concussion + pulmonary
Pulmonary complications occur with severe sensorimotor and cognitive system deficits
Severe concussion manifestations
Pupillary changes, cardiac and respiratory symptoms, decorticate or decerebrate posturing, and abnormal reflexes
Severe concussion + IICP
IICP appears 4 to 6 days after injury
Cerebral laceration means…
There is a tearing of the brain associated with DAI
Cognitive deficits associated with TBIs
-Hydrocephalus
-Sensory-motor disorders, including pain, paresis, and paralysis
-Loss of coordination
Post concussion syndrome
-Weeks to months
-Headache, dizziness, fatigue, nervousness/anxiety, irritability, insomnia, depression, inability to concentrate and forgetfulness
Careful monitoring for first 24 hrs to ensure no bleeding
Post traumatic seizures
-Most often in open brain injuries
-Occurs within days of event and up to 2-5 years
Chronic traumatic encephalopathy
-Progressive and dementing disease that develops with repeated brain injury
-Leads to violent displays of behaviors
Monitor which levels in TBIs
Na+
Traumatic brain injury assessment (neuro)
-LOC, monitor for deterioration to worst case, coma & unresponsive, pupillary changes unilaterally and bilaterally, equal, abnormal in shape, size, reactivity
-Does the patient follow commands, MP weak/strong, equal upper/lower; abnormal posturing, flaccid
-Headache, aVision
TBI CV assessment
bradycardia & widening pulse pressure (sign of Cushing’s triad), HTN, aPerfusion, cap refill, pulses
TBI resp assessment
Monitor for changes in respirations: Bradypnea, tachypnea, irregular, Cheyne’s stoke present or absent
TBI renal assessment
Urine output, is it > or < 30 cc/hr, colour, consistency, frequency, 24 hour fluid balance
Spinal cord injury (SCI) common causes
Common causes include MVCs, falls, work place related injuries, sports injuries, medical conditions and violence
Pathophysiology of SCIs
-Initial injury; primary & secondary injuries
-Spinal and neurogenic shock
SCI + initial injury + primary vs secondary injuries
-Occurs d/t compression by bone displacement, tumor or abscess or from interruption of blood supply to the cord
-Primary injury: Occurs with a fracture of dislocation of the spinal cord column
-Secondary injury: Involves vascular dysfunction, edema, ischemia, electrolyte shifts, inflammation, free radical production and apoptotic cell death
Spinal shock
-Characterized by decreased reflexes, loss of sensation and flaccid paralysis below the level of injury; lasts days to months
-Pt can recover from spinal shock
Neurogenic shock
Caused by loss of vasomotor tone and manifested by HYPOTENSION, BRADYCARDIA, and hypothermia.. All other forms of shock result in tachycardia
MOA of SCI
Flexion, hyperextension, flexion-rotation, extension-rotation and compression
Flexion SCI
Forward dislocation resulting in damage to the spinal cord & ruptured posterior ligaments
Hyperextension SCI
Ruptured anterior ligament and compressed posterior ligaments
Compression fracture SCI
Compression of spinal cord & fractured vertebrae
Flexion-rotation SCI
Displacement of vertebrae
Tool used to assess spinal cord injuries
Association impairment scale, r/t sensory & motor function
Injury below T6
Paraplegic
Injury above T6
Quadraplegic
T6 is where
At the nipple line
SCI degree of injury
-Central cord syndrome
-Anterior cord syndrome
-Posterior cord syndrome
-Brown-Sequard syndrome
Central cord syndrome
-Complete loss of arm movement, partial leg function & sensation remains
-GI/GU are partially spared
-Recover motor & sensory slowly in legs & trunk
Anterior cord syndrome
-Complete loss of movement, partial or complete loss of sensation except to pressure & vibration which remains intact
Posterior cord syndrome
-Movement & sensation preserved
-Difficulty walking
Brown-Sequard syndrome
-MP impaired on injured side, pain and temperature sensation remain normal.
-MP normal on unaffected side, pain and temperature sensation are reduced or absent.
-Having 1 leg that functions is very helpful in ADLs
SCI resp manifestations
> T6; PE, difficulty coughing
SCI CV manifestations
->T6; bradycardia & hypotension d/t peripheral vasodilation, hypovolemia, & ortho hypotension
SCI GU/GI manifestations
-GU; retention
-GI; >T5; hypomotility causing paralytic ileus, gastric distention, may need to disimpact
SCI thermoregulation
Cannot regulate temp in high cervical injuries
SCI peripheral vascular conditions
Virchow’s triad, DVT
Autonomic dysreflexia/hyperreflexia
-EMERGENCY HTN event
-Caused by noxious stimuli; once stimuli is removed the problem is resolved
-Sudden HTN (240/12 or higher than usual ie. 100/70 to 140/90)
-Management is to remove stimuli
Manifestations of autonomic dysreflexia/hyperreflexia
-Severe headache
-Flush face & neck with upper chest perspiration
-Appears anxious, cold & goose bumps on lower extremities
Slide 66
CVA pathophysiology
-Interruption of blood flow in the brain
-Classified as global hypo-perfusion, ischemic or hemorrhagic stroke
-Caused by: Impairment in autoregulation, changes in blood flow, increased CO2 & ICP, low arterial levels, & aBP
Types of CVA
-Ischemic, hemorrhagic, r/t hypoperfusion
TIA is a..
-Precursor to stroke
-Last less than an hour, unable to move
Ischemic stroke
-Classified as a TIA
-Transient episode of neurological dysfunction
-Acute infarction of the brain
-Symptoms last less than 1 hour, most resolve on their own
-Result of a micro-emboli
Manifestations of an ischemic stroke
Temporary loss of vision, transient hemiparesis, numbness or loss of sensation, or a sudden inability to speak
Types of ischemic strokes
-Thrombotic; occurs from injury to a blood vessel and formation of a clot, most commonly the result of atherosclerosis
-Embolic stroke; occurs when an embolus lodges in an occluded cerebral artery
Thrombotic stroke pathophysiology
-Blood vessel becomes narrowed or occluded causing primary injury (no flow) and secondary injury (low flow)
-Lacunar stroke refers to a stroke from an occlusion of a small penetrating artery
Thrombotic stroke manifestations
-Motor hemiplegia, sensory stroke, contralateral leg and face weakness with arm and leg ataxia, & isolated motor or sensory stroke
Embolic stroke associated conditions
Heart conditions
Hemorrhagic stroke pathophysiology
-Result of bleeding into the brain tissue (intracerebral hemorrhage) or into the subarachnoid space (subarachnoid hemorrhage-SAH)
-Ischemic strokes can lead to hemorrhagic strokes
CVA manifestations
-Motor function; swallowing, respiratory, gait
-Communication; broca’s (expressive) & Wernicke’s (receptive) aphasia, amnesia and global aphasia
-Affect & intellectual Function
-Spatial-Perceptual Alterations; anosognosia, homonymous hemianopia, agnosia, apraxia
Anosognosia
Know they have a problem but deny it
Homonymous hemianopia
Visual changes
Agnosia
Cannot recognize an object by sight, touch or hearing
Apraxia
Cannot complete a task with sequential events
Left hemisphere is…
Most dominant for language in those that are right handed and some that are left handed
Amnesia in terms of speech
Cannot find the correct word
Global aphasia
Expressive & receptive issues combined
Dysarthria
Impaired muscles used when speaking
Post CVA manifestations
Depression & impaired memory
Left brain stroke
Impaired memory, language & tend to be cautious when doing things
Right brain stroke
Impulsive nature
Slide 75
CVA neuro assessment
LOC, Canadian Neurological Scale, cognition, motor abilities (unilateral, contralateral sensory and motor weakness)
-Cranial nerve function, sensation, proprioception, cerebellar function
-NVS, pupillary changes, slurred speech, spasticity, seizures
CVA CV assessment
hypertension, tachycardia, bruit, aPerfusion
CVA resp assessment
Monitor airway protection; dysphagia, aspiration pneumonia, loss of cough reflex, labored, apnea
CVA GI/GU assessment
-GI: Loss of gag reflex, decreased or absent bowel sounds, nutritional intake
-GU: Urine output (monitor for dehydration if unable to swallow), frequency, incontinence
Canadian neurological scale
-Slide 77
-For stroke patients
Anterior cerebral artery causes which conditions when occluded?
-Hemiplegia on the contralateral side of the body, greater in the lower than upper extremities
Occlusion of the middle cerebral artery causes
Aphasia dominant hemisphere & contralateral hemiplegia
Posterior cerebral artery occlusion causes
Visual & sensory loss and contralateral hemiplegia if the cerebral peduncle is affected
Slide 79
Pathophysiology of cerebral aneurysms
-Sac like out pouching of a cerebral artery
-Large number of people have intracranial aneurysms which are innocuous and do not bleed
-More often in women than men (ratio 3:2)
-If ruptures, usually results in SAH
-Outcome of ruptured aneurysm is poor, only 1/3 who have SAH recover without a major disability
Where cerebral aneurysms form
-Located at bifurcations and branches of arteries at base of the brain and circle of Willis
-85% develop at the anterior part of the circle of Willis
Classification of cerebral aneurysms
Classified by size & shape (small to 15mm & giant from 25 to 50 mm)
Shape classifications of cerebral aneurysms
-Berry, saccular
-Traumatic, myotic (infectious)
-Dissecting
Cerebral aneurysm manifestations before rupture
-Dilated pupils, ptosis (eye droop), diplopia, pain above and behind left eye
-Localized headache, N/V
Cerebral aneurysm manifestations after rupturing
-Violent/explosive headache
-Immediate loss of consciousness
-Vomiting
-SAH (subarachnoid hemorrhage) related deficits
Vasopasm + cerebral aneurysm
-Narrowing of a cerebral blood vessel
-30% of patients experience vasospasm post rupture
-Spasm causes decreased cerebral perfusion further causing ischemia and/or infarct
-Unknown etiology
Manifestations of vasospasms in cerebral aneurysms
aLOC, paresis/paralysis, cranial nerve deficits & aphasia
Early signs of cerebral aneurysms
-aLOC and pupillary responses/ocular movements
-Weakness on one side of the body or in one extremity
-Constant headache that increases in intensity with movement or straining
Later signs of cerebral aneurysm: IICP
-LOC diminishes to point of comatose
-HR, resps, temp, & BP rise. Pulse pressure widens (distance between the diastolic and systolic), pulse fluctuates between bradycardia and tachycardia within minutes
-Cheyne-stoke respirations
Pathophysiology of meningitis
-Caused by bacteria, viruses, fungi, parasites or toxins
-May be acute, subacute, or chronic
-Meningococcus can reside in nasopharynx and throat, asymptomatic
-Bacterial organisms grow/replicate in the CSF releasing endotoxins or cells wall fragments; CSF circulation spreads it
-Contact droplet precautions
Incidence of meningitis
Highest incidence among children and young adults
Dx & tx of meningitis
-Diagnose using lumbar puncture (LP)
-Prophylactic antibiotics
Bacterial meningitis manifestations in children <2 years old
-Fever, anorexia, vomiting, diarrhea
-Listlessness, pale, look disinterested
-Bulging fontanels & high pitch cry
Manifestations of bacterial meningitis in children & young adults
-Headache, stiff neck, pain with knee and neck movement
-Fever, LOC deterioration, generalized convulsions,IICP & cranial nerve dysfunction
Nursing assessment of bacterial meningitis
-Nutrition, fluid and electrolyte imbalances, transmission
-Brudzinski sign; chin to chest, kernels sign; hamstring pain
Brudzinski & kernigs sign assess for
Subarachnoid involvement
Encephalitis pathophysiology
-Acute febrile illness, usually viral in origin
-Most common form associated with mosquitos born viruses or herpes simplex type 1, may follow vaccinations with a live vaccine
-Edema, necrosis with or without -Hemorrhage & IICP develops
Clinical manifestations of encephalitis
Fever, headache, stiff neck, aLOC (from disorientation to coma)
Nursing assessment of encephalitis
Full neuro assessment, VS, aLOC, gait & speech
General aspects in a neuro assessment + paediatrics
-Gain info about infants/toddlers by observing reflexes
-As they age they develop increasingly complex gross and fine motor skills and develop communicative behavior.
-Delayed developmental milestones helps identify at risk children
Physical neuro assessment + paediatrics
-Size and shape of the head, sensory responses, symmetry in movement
-Inability to suck or swallow, asymmetrical smile, abnormal eye movement, twitching & crying
Major features associated with neurological abnormalities + pediatrics
-Decreased LOC
-IICP
-Seizures, hypotonia, abnormal head size
Moderate features associated with neurological abnormalities + pediatrics
-Persistent deviation of head and eyes
-Asymmetrical posture or movement
Minor features associated with neurological dysfunction in pediatrics
-Jitteriness, poor feeding & abnormal head shape
IICP in pediatrics
-Often caused by a TBI
-Also occurs in hydrocephalus, brain tumors, & intracranial infections
-Therapy should be directed at both reducing ICP & reversing its underlying causes
Intracranial volume is made up of
-Brain, CSF & blood; these volumes must remain ~ the same at all times
Symptoms of IICP
-Headache (earliest symptom)
-Decreased LOC
-Vomiting & pain coming in waves
-aVision, focal physical weakness or loss of coordination
Signs of IICP
-Papilledema, retinal hemorrhage, scratching head
-Infants; split sutures or bulging fontanel
-Dilated pupil, unilateral on the same side as the lesion
-LOC can range from irritability to coma
-Hyperreflexia, hypertonia, bradycardia & respiratory depression are late signs
Nursing assessment of IICP
-GCS & pediatric coma scales
-PERRLA
-Spontaneous activity, posture & response to pain
-Posturing (flexion/extension)
Investigations for IICP
-CT & lumbar puncture
Hydrocephalus
-Syndrome resulting from CSF disturbances
-Fluid accumulation causes enlargement and dilation of the ventricles of the brain & IICP
If left untreated, hydrocephalus can
Lead to severe brain damage.
Tx of hydrocephalus
Surgical shunting procedure to drain CSF
Causes of hydrocephalus
Congenital defects (e.g. spina bifida), secondary to infection (e.g. meningitis), or trauma
Nursing assessment of hydrocephalus
-Increased head circumference, veins
-Bulging fontanels & crying
-“Setting sun” sign (eyes look like a setting sun)
-Delayed development, reflexes & poor feeding
Causes of pediatric seizures
-Structural: Trauma, malformation, intracranial hemorrhage
-Ingestion/drug withdrawal
-Metabolic: Hypoxemia, hypoglycemia, hypo-hypernatremia, hypocalcemia, & hypomagnesemia
-Infections & familial
Nursing interventions for seizures
-Monitor length, ABC, reps, pulse, diaphoretic or dry, what type, evacuated bladder/bowel
-Cannot protect own airway for >5 minutes (intubation required)
Atastic seizure
Sudden loss of muscle tone that may be focal (eg. head nod), hemibody or generalized (fall or drop attack)
Behavioural seizure
Abrupt change in behaviour w/o other overt features (quiet-hyper motor), occasionally autonomic signs (pallor, cyanosis)
Clonic seizure
Clonic jerking of extremeties or eyelids, occasionally followed by tonic posturing
Infantile spasms
May be myoclonic or brief tonic flexor or extensor spasms. Often occur in clusters
Tonic seizure
Symmetric or assymetric posturing (occasional fencer posture), may be followed by focal or generalized clonic activity
Versive seizure
Forced & sustained tonic deviaton of the eyes that is associated with ipsilateral turning of the head & rotation of the trunk
Benign febrile seizure epidemiology
-Most common cause of seizures in children
-6 months - 5 years
-Twice as common in boys
-Possibly genetic
Etiology of benign febrile seizures
-Unknown
-Transient problems occur exclusively in the presence of high spiked fevers
Manifestations of benign febrile seizures
-Rapid rise in temp
-No neurological or developmental delay before or after seizure
-No hx of non-febrile seizures, no infection before or after
-<15 minutes
-Generalized tonic-clonic, symmetric
-Does not recur in a 24hr period
Investigation of benign febrile seizures
-Clinical diagnosis
-Septic work up including LP if meningitis is suspected
