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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

Full consciousness

Awareness of self environment and response to environment


-Decrease in any of these decreases the LOC


Involving arousal and awareness


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

Awareness

Awareness involves the thought process

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


Structural causes for a change and arousal

Infection, vascular, neoplastic, traumatic, congenital, degenerative, metabolic

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

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

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

Psychogenic reasons for arousal disorders

Not a common cause or physical cause


Psychiatric disorder implying unconsciousness, but the person is physiologically awake

5 clinical manifestations that Aid in determining the extent of brain dysfunction

LOC


Pattern of breathing


Pupillary reaction


Oculomotor response


Motor response

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)

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

Pupillary response

-Control for pupils is located near brainstem area that controls arousal


- helps determine level of brainstem dysfunction

Condition of patient versus pupil response

Oculomotor response

Choose changes at various levels of brain dysfunction in comatose state

Metabolic coma

Ocular reflexes present

Barbiturate hypnotic coma

Ocular reflexes absent

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

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

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

Possible outcomes of disability

-rocovery of consciousness


-residual cognitive function


-psychologic function


-vocational function

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

Cerebral death

-death of cerebrum but not the brainstem and cerebellum


-permanent and unable to respond

Coma

Eyes closed, no voluntary movement/speech

Persistent vegetative state

Awareness of self but no cognitive function


Sleep/wake with spontaneous eye opening

Minimally conscious state

May follow simple commands, gesture, blinking, smiling, speech

Locked-in syndrome

No voluntary movement except eyes


Thought and arousal are intact

Alterations in awareness

Can involve cognitive functions, simple to complex


Selective attention deficit


Memory deficit: amnesia


Executive attention deficits

Selective attention deficit

Inability to select and process information


-seizures, parietal lobe confusion, subdural hematoma, stroke, tumor, late alzheimers frontotemporal dementia

Memory deficit amnesia

Retrograde


Anterograde

Retrograde amnesia

-Gross loss of past memories or factual data OR loss just prior to the trauma/disease


-concussion


Anterograde amnesia

-Can recall distant past but unable to form new memories or retain data since the trauma/disease


-Concussion

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


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

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

Seizure

Sudden disordered discharge of cerebral neurons, temporary altering brain function and level of arousal

Convulsion

Seizure activity in which muscles contract-relax in a tonic-clonic movement

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

Types of seizures

Partial seizures


Generalized


Unclassified

Partial seizure(begins locally)

-Simple: no LOC-Complex: change in LOC-Secondarily generalized: begins locally but evolves into generalized tonic-clonic

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)

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

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

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

Data processing problems

Agnosia


Dysphasia/aphasia


AgnosiaDysphasia/aphasiaAcute confusion (delirium)Dementia


Acute confusion (delirium)


Dementia

Agnosia

-Inability to recognize shape/form of objects: tactile, visual, auditory-Most common cause is CVA

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

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


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

Dementia verses delirium

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

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


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/

Alteration in Cerebral Hemodynamics

 -Secondary
brain injuries occur after a brain is injured and include alterations in 
  -Cerebral blood
flow 
  -Intracranial
pressure 
  -Oxygen
delivery

-Secondarybrain injuries occur after a brain is injured and include alterations in


-Cerebral bloodflow


-Intracranialpressure


-Oxygendelivery

(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

Alterations incerebral blood flow

-Inadequatecerebral perfusion


-Normalcerebral perfusion with elevated


intracranial pressure


-Excessivecerebral blood flow

CPP required after brain injury

>70 mmHgwhile intracranial pressure is usually 1-15 mmHg

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

Increased intracranial pressure has how many stages?

4 Stages

Stage 1

-Vasoconstrictionof the cerebral venous


system; may be able to compensate for the


pressure


-Few symptoms may be seen

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

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

Stage 4

-Brain tissueshifts and the compartment


of highest pressure herniates


-Unevendistribution of pressure


-Herniated area suffers further ischemia and hypoxia

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

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

Treatment (Hydrocephalus)

Surgery viaNeurology/Neurosurgery

Care Issues(Hydrocephalus)

-Enhance psychomotor development


-Large head causes difficulties with milestones


-Monitor forshunt infection/malfunction


-Ventriculitis, sepsis


-Increased ICP

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

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

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

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|

Alterations in Muscle Movement

Dysfunctionsin CNS alter muscle innervation


Dopamine alsohas affects on muscle movement


Paresis


Paralysis

Dysfunctions in CNS alter muscle innervation

Notnecessarily associated with mass or strength -Does not haveadequate strength of +5

Dopamine also has affects on muscle movement

-Too little:akinesias


-Too much:chorea, tardive dyskinesia

Paresis

Weakness,partial paralysis with partial loss of muscle power

Paralysis

Loss of motorfunction; inability to overcome gravity

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

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

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

Poliomyelitis

-Severeinflammation or motor neurons from polio virus


-Some may dieand lead to paralysis

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

Bulbar Palsy

-Involves theCNs from the bulb: CN IX, X, XII


-Paresis/paralysisof jaw, face, pharynx, and tongue

Hyperkinesia

excessivemuscle movements

Dyskinesia

"abnormalinvoluntary movements"


-TardiveDyskinesia


-Movement ofthe face, trunk and extremities


-Mostcharacteristic is continual chewing with lip smacking


-Often as aSide Effect of phenothiazines

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)

(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

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

Abnormal Movements Hypokinesia

Loss ofvoluntary movement even though consciousness is preserved, along with normalperipheral nerve and muscle function

Akinesia

-Decrease involuntary movements


-Defect inextrapyramidal system, involving dopamine

Bradykinesia

-Slowness ofvoluntary movements with difficulty -Initiatingmovement


-Continuingmovement smoothly


-Performingtasks at the same time or one after


the other

Loss of associated movement

Expressionlessface, statue posture, no speech inflection, spontaneous gestures

Parkinson Disease (hypokinesia)

Commondisorder of movement (1 in 272)

SecondaryParkinson Disease

-Caused by adisorder other than Parkinson


-Head trauma,infection, neoplasm, toxins, drug


intoxication


-Drug-inducedis usually reversible

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)

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

Disorder of Stance


DecorticatePosturing

-Brainstem is
not inhibited by the cerebral cortex motor area   
  -Flexed at the
elbows 
   and close to body 
  -LE extended

-Brainstem isnot inhibited by the cerebral cortex motor area


-Flexed at theelbows


and close to body


-LE extended

Disorder of Stance


Decerebrate Posturing

 -Severe injury
to brain and brain stem   
  -Overstimulation
of 
   postural righting and 
   vestibular reflexes 
  -Increased tone
in 
   extensor muscles

-Severe injuryto brain and brain stem


-Overstimulationof


postural righting and


vestibular reflexes


-Increased tonein


extensor muscles

Disorders of Expression

All involvethe motor aspect of communication

Hypermimesis

Pathologiclaughter(right hemisphere)or crying (left hemisphere)

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

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

Brain Trauma Causes

-Transportation-related(MVA, PVC, bike, skateboard)


-Falls


-Sports-related


-Violence

Brain Trauma Improved Survival Rates due to

-Advancementsin safety measures


-Reduced timeto medical care


-Trauma centers


-Improvedon-scene medical management

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

Mechanisms of Brain Injury

Primary


Secondary


Tertiary (days or months later)

Primary

Caused byimpact: neural injury and vascular responses

Secondary

-Indirectconsequence of the injury, causing further neuronal injury or death


-Alteredcerebral blood flow, hypoxia, ischemia,


inflammation, edema, IICP, herniation

Tertiary

-Consequence ofprimary and secondary injury


and systemic complications that contribute to


further brain injury


-Pneumonia,fever, infections, immobility

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

Brain Trauma Diffuse Axonal Injury

-Involving morethan one area of the brain


-50% of allbrain trauma with 33% of brain


injury deaths


-More disabledsurvivors2

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)

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

Brain Hematomas



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

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

Categories of DAI

Mildconcussion


Classiccerebral concussion


Mild diffuseaxonal injury


Moderatediffuse axonal injury


Severe diffuseaxonal injury

Mildconcussion

-No LOC, butconfused for several minutes


-Possibleretrograde amnesia, headache and not


“being themselves” for days

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

Mild diffuseaxonal injury

Decerebrate ordecorticate posturing in 30% with prolonged stupor

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

Severe diffuseaxonal injury

Outcome morebleak: severely compromised skills, inability to learn, behavior problems

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

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

4 Classification of Spinal Cord Injuries

SimpleFracture spinous process


Compressed Vertebral Fracture


Comminuted(burst) fracture


Dislocation

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

Spinal Shock

-Reflexfunction below the lesion is lost


-Skeletalmuscles


-Bowel/bladder/sexualfunction


-Autonomiccontrol


-Lasts days to3 months


-Reflexes,spasticity and hyperreflexia begin to


reappear

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

Major Dermatomes to know

 -C3: neck 
-C6: radial
side of arm 
-C8: ring and
small finger 
-T4: nipples 
-L1: inguinal  
-L4: knee 
-L5: shin,
ankle, foot 
-S5: anal area

-C3: neck


-C6: radialside of arm


-C8: ring andsmall finger


-T4: nipples


-L1: inguinal


-L4: knee


-L5: shin,ankle, foot


-S5: anal area

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

Degenerativedisc disease

-Disk can herniate and pinch the spinal nerve


-Most have nofunctional incapacity due to pain

Spondylosis

Defect in thelamina or neural arch of vertebra

Spondylolisthesis

Vertebraslides forward onto the vertebra below

Spinalstenosis

Narrowing ofthe spinal canal

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

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

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

Focal Signs- Frontal Lobe

Gait, musclemovement, seizures

Focal Signs- Parietal Lobe

Sensation andproprioception

Focal Signs- Temporal Lobe

Auditory,hallucinations, partial seizures and memory

Focal Signs- Occipital

Visual:blindness, agnosias, and visualhallucinations

Focal Signs- Limbic

Memory anddecision-making skills

Focal Signs-Cerebellar

Balance andcoordination

Focal Signs-Brainstem

Variedsensory-motor issues and CNS

Focal Signs- Spinal Cord

unilateralparalysis with contralateral loss of pain sensation

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

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

Thrombotic vs Embolic vs Cerebral Hemorrage



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

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

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

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

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 -

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

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

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

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]

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

Bacterial Meningitis > 2 years

•Fever,lethargy


•Headache


•Vomiting


•Seizures –late sign


•Nuchalrigidity


•+ Kernig and Brudzinski

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

Aseptic Meningitis

•Causes


•Virus:measles, mumps, herpes, enteroviruses


•Leukemia


•Onset isabrupt or gradual


•Similarclinical findings but generally mild


•Self-limitingdisease


•Treatment issymptomatic and supportive

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

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

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

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

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

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?

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

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



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

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

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%:

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

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