Test 2

Quiz yourself by thinking what should be in each of the black spaces below before clicking on it to display the answer.

Help!

Question

Answer

Weber's Syndrome - structures involved

Brainstem: Midbrain: 1. Descending corticospinal; 2.corticobulbar

🗑

Weber's Syndrome - manifestations

1. contrlateral hemiparesis; 2. ipsilateral 3rd CN palsy(ptosis, no eye movement up, down, or medially; and if fibers of EW nucleus pupollary dilation

🗑

Bendikt's Syndrome - structures involved

Brainstem: Midbrain: 1. 3rd CN; 2. Red Nucleus

🗑

Bendikt's Syndrome - manifestations

1. ispilateral 3rd CN palsy; 2. contralateral ataxia; (can result from a midbrain stroke involving the 3rd CN traveling near the RN. A lesion of the RN interrupts fibers from the opposite cerebellar hemisphere

🗑

Parinaud's Syndrome

Damage to superior colliculus; imparied upward gaze and convergence

🗑

Pons - Ventral and Dorsal regions

Ventral: corticospinal, pontine nuclei, transverse fibers; Dorsal region: nuclei of CN. medial lemniscus, RAS, Locus Coeruleus

🗑

Dorsolateral infarction of the Pons

Causes: vascular lesion or tumor; manifests: contrlateral loss of paon, temperature(face not affected), ipsilateral cerebellar ataxia, deafness, nystagmus

🗑

Paramedian infarction of the Pons

CN 6, 8; medial lemniscus; medial lemniscus: touch and proprioception on opposite side

🗑

Millard Gubler syndrome

Unilateral basilar infart; contralateral hemiplegia; CN 6,7; central pontine meylinolysis

🗑

Medulla - Structures

Anterior, olive, nuclei for CN 9-12, reticular formation. vasomotor center, respiratory center

🗑

Lateral medullary syndrome(wallenberg syndrome)- causes

Brainstem CVA-occlusion of posterior inferior cerbellar artery(branch of Vertebral artery)

🗑

Lateral medullary syndrome(wallenberg syndrome) - structures involved

Spinothalmic tract: contralateral loss of pain and temp below level; inferior cerebellar peduncle: ispilateral ataxia

🗑

Basial infarction(Locked in Syndrome)

Bilateral damage; corticospinal damage; Spinothalmic may be ok

🗑

Cerebellum - General Function

coordinates voluntary muscle activity; eq(Vestibular aparatus); tonicity; Modulates movements: especially rapid, helps time sequence events, monitor and makes adjustments, compares actual with intended(cortex and muscle afferent input)

🗑

Cerbellum - Structures

Cerebellar heispheres: anterior and posterior lobes; vermis(controls axial body); Nuclei: dentate(biggest;output), fastigial VC - eq, interposed spinocerebellum - input from spine

🗑

Superior Cerebellar Peduncles(input,output)

Rubiospinal Tract - Input(monitors movement): ventral spinocerebellar(contra prdominately, can ascend bilaterally from tendons) lower limbs(below L2-3); output(corrects movement): Dentate to contra RN tp cpntra cortex to contra SC(same side of input)

🗑

Middle Cerebellar peduncles

Pontocerbellar tract - intended movement from the cortex to pons to cerebellum

🗑

Inferior Cerebllar Peduncles(input,output)

input: dorsal spinocerebellar (C8-L3) (T1-L2 Clarkes nucleus) to vestibular(can influence both sides) to reticular formation(afferent(VF and ICP) and efferent(MN) to inferior olivary nuclei; Output Vestibular and RAS (fastigiobulbar tract)

🗑

Ataxia

Major manisfestion of cerebellar disorders, disorganized gait

🗑

Anterior cerebellar lobe dysnfunction

nutritional deficiencies(B12), EtOH, broader gait

🗑

Posterior cerebellar Vermis syndrome

brain tumors(children(80% below tentorium) with meduloblastomas or ependymomas 3,4th ventricles); profoundly disturbed gait and inability to stand without swaying(truncal dystaxia)

🗑

Cerbellar hemisphere syndrome

ipsilateral defecits; tumors or abcesses, uncoordination or ipsilateral limbs; Hands Tremor

🗑

Hands Tremor

Hypotonia(no resistnace to movement); Asynergy(decrease in coordination); Nystagmus; dysartrhria(speech/chew); Station and gait; intention tremor

🗑

Spinal Nerves/root types

A alpha 1a or 1b(fastest); A beta(II); A delta(III) sharp pain; A gamma; B; C (IV) small unmyelinated (dull constant)

🗑

Spinal cord - grey matter

Lamina 1-4 dorsal horn(substancia gelatinosa(I+II, fetanyl target); VI thoracolumbar, craniosacral (clarks T1-L2)+ANS; lamina IX: alpha + gamma MN(c3-6 phrenic Nucleus; lamina X surrnounds CNS

🗑

CSF - porperties

Clear wattery liquid in subarachnoid(pia and arach) contains small amount of protein sugar and electrolytes(not the same as plasma) 100-150mls, 70-180 mmH2O(10mmHg); produced by choroid plexus

🗑

CSF - Ciruculation

later Vent -> interventricular foramen - > third vent -> cerbral aquaduct -> fourth vent -> spinal cord and brain -> foremen of magendi and luschka -> arachnoid villi(pressure gradient leaves by bulk flow)

🗑

CSF - Function

preserves homeostasis - proten content(maintains oncotic pressure), buoyancy for brain, lymph system for brain

🗑

BBB

capillaries have tight junctions between capillary endothelial cells, glial foot processes of astrocytes encase caps; cap endo have high number of mitochon for transport out; substances that can cross: small, lipid soluble, carrier mediated transported

🗑

Communicating hydrocephalus

overproduction of CSF(adolescence), blood, or tissue, route is ok; montly csf taps

🗑

Obstructive hydrocephalus

obstruction of flow, tumors, scarring, lateral vent enlarges

🗑

Supratenorial Herniation

uncal - compression of 3rd CN, ipsi or if severe contra; central - pressure strain down bilat 3rd CN palsy

🗑

Infratentorial Herniation

trans formenal, pons - apneusis(sustained gasping inspire, short inefficient expire; top of medula - clustered, medula - gasping

🗑

Doll's Eyes(occulocephalic reflex)

eyes still stay straight when tuened(good vestibular, EOM; no turn brain damage midbrain and pons

🗑

Oculuvestibular reflex (cows)

cold water in ear, looks slowly to same side, nystagmus to the other, warm opposite; nothing brain damage, one eye damage at pons and midbrain

🗑

Compensation for Increased ICP

decrease blood within CV->cerebral vasoconstriction-> cerebral hypertension-> Cushing refelx(peripheral vasoconstriction) increase in MAP; cerbral perfusion pressure=MAP-ICP; Clinical signs increased BP widening pressure pulse, decrease HR

🗑

Increased ICP, failure to compensate from Cushings reflex

ICP still increasing->extreme hypoxic->decompensate-> vasodilate-> inc. dienceph pressure, breathing changes(cheyne stokes)-> inc. in upper brainstem pressure-> central neurogenic hyperventialtion(deep rapid breath remove CO2 from blood to cause vasocon

🗑

CSF Infections

Menigitis: acute(BCT), Subacute or chronic(aseptic, viral,fungal,TB); Encephalitis: acute(BCT, Viral), chronic(fungus, yeast, TB), Space occupying lesions: brain(immuno comp, iv drugs), epidural abcess(iatro), subdural empyema(iatro); encephalomyelitis

🗑

Menigitis

inflammation involving the archnoid, pia mater and CSF in the subarachnoid space; extends throughout the subarachnoid space around the brain, spinal cord and ventricles

🗑

Viral Menigitis

Benign, rarely fatal, self limiting; enterovirus(80%), mumps, EBV, Herpes(rare but serious); no preventative or tx except herpes virus; HSV and VZV needs systemic antivirals(AIDs)

🗑

BCT Menigitis - neonates

Group B Strept(vag), Listeria, E. coli

🗑

BCT Menigitis - infants and children

used to be H. flu(HIB)<5%; S. pneumo, N. Menig, S. Aureus, Listeria

🗑

BCT Menigitis - Normal adults

S. pneumo(30-50%), N menig(10-35%) higher morbidity

🗑

BCT Menigitis - post-surgical

pseudomonas, S. Aureus

🗑

Acute Bacterial Menigitis Risk Factors

Extremes in age, crowded conditions terminal complement deficincy(c6,7,8,9)N. men, splenectomy(S. pneumo), SCD, EtOHism/liver damage/cirrhosis, CSF leakm CSf shunt, DM, Sinusitis, OM, brain abcess, Recent Neurosurgery, immunosuppression

🗑

Acute Bacterial meningitis Pathophysiology - Hematological Route

Lung(S. Pneumo 31% deafness), Skin and subg tissue bone/osteomyelitis(S. Aureus), intestinal: e. coli

🗑

Acute Bacterial meningitis Pathophysiology - Contiguous(direct) Route

Ear/OM(infants), URI(N. Mening 11% deafness)

🗑

Acute Bacterial meningitis Pathophysiology - direct entry Route

trauma/Sx/LP (prophylactic AB)

🗑

Acute Bacterial meningitis Pathophysiology - Virulence Factors

Bct LPS activates IL-1, Il-8, and NO from endo and Astros cause leaky vessels allowing for disem. IgA proteases allow adherence to mucosa, Capsule are anti-phagocytic

🗑

Acute Menigitis Manisfestations of BCT

Onset: Rapid(25%)vSlow(75%); Fever>90%; headache 90%, menigismus 85%, Lethargy 80%, petechia/purp(50% if N. menin); vomit(30%), seizures(GM/inflam MC 30%); focalneurosigns(6 cn palsy)25%; hemiparesis, papolledema 1%, photophobia/blurred; no accomidation

🗑

Kernigs and Brudzinski signs

low sensitiveity buy high specifity to ABM; try to extend lower leg causes back pain; bring legs in to when neck flexed

🗑

Acute Bacterial meningitis physical findings needed for a diagnosis

Fever, menigismus, and altered mental status

🗑

Acute N Menigococcal Menigitis(prognosis and physical findings)

Prog: 5-10% mortality, septic 12-40%; isolate after Dx(droplet precautions); purpueric rash/DIC(40-90%) 12-36 hours may lead to pupura fulminans(systemic) increased ICF(headache, profectile vomit, papilledema/swollen disc/ av nicking(late sign)

🗑

Acute Bacterial meningitis physical findings for adults(early vs late)

Early: headache, vommiting, papilledema; Late lethargy, uni/bi 6 CN Palsy, transtentorial or transforaminal syndromes

🗑

Acute Bacterial meningitis physical findings for children(early vs late)

early: enlarged head; Late: lethargy or hyperirritiable, failure to thrive, vommit; bulging of anterior font., distention of scalp veins, seperation of cranial sutures, setting sun syndrome, papilledma. uni/bi 6 cn palsy, transtentoral and trandforam symp

🗑

Transtentorial Herniation - early signs

ipsilateral 3rd nerve pals; increasing stupor; contralateral hemiparesis; (ipsilateral occurs as a false localizing in 20% of cases; corticol blindness

🗑

Transtentorial Herniation - late signs

coma, irregular respiration(cheyne stokes, CNH; uni;/bi decorticate posutring

🗑

Transtentorial Herniation - Pre-terminal signs

Bilateral dilated fixed pupils; loss of VO reflex(dolls eyes); no deep tendon refexes; EEG-Flat

🗑

Transforamenal Herniation - early signs

head tilt, nuchal ridgity,subocipital tenderness

🗑

Transforamenal Herniation - late signs

respiratory arrest; stupor to coma; uni/bi decerebrate posturing

🗑

Transforamenal Herniation - Pre-Terminal signs

circulatory collapse

🗑

Lumbar puncture characteristics

pressure, clarity, presence of microorganisms, leukocytes, RBC, conc. glucose, protein, gamma globulin, lactic acid, presence of endotoxins and bct antigens

🗑

LP protocol

obtain before imaging if ABM suspect, repeat 8-12 hr if Dx is uncertain; pts with neuro findings or papilledma usually don't have ABM image then LP; with brain abscess, subdural empyema, subdural LP bad!; rel. contra: infect of skin, sig bleed disorder

🗑

Lumbar puncture pressure + tubes

normal:50-195mmH20; ABM: 90%>180mm, 20%>400mm, 5%.500mm; Tube: 1 cell count with diff, 2 glucose,protein, 3 gram stain, 4 viral cultures

🗑

Lumbar puncture normal levels

WBC: 0-5; %PMNs: 0-15%; Glucose: 45-65; CSF Blood glucose .6; Protein: 20-45

🗑

Lumbar puncture ABM

WBC: >1,000; %PMNs: 90%; Glucose: <40; CSF Blood glucose <.4; Protein: >150

🗑

Lumbar puncture Viral

WBC: not as high as BCT; %PMNs: <50%; Glucose: 45-65%; CSF Blood glucose .6; Protein: 50-100

🗑

Acute Bacterial Meningitis empiric Treatment

early rec, id and rapid intiation, isolation, empiric AB(IDSA): <1 month amp+cefotaxime or aminoglycoside; 1-23 months + 2-50yers: vanco + 3rd ceph; >50yrs vanco+3rd ceph+amp

🗑

Acute Bacterial Meningitis tailored Treatment

S. Pneumo, N. Mening, Listeria pen G or amp; H. flu amp; Dexamenthasone stops deafenss: .15mg/kg every 6 hr for 2-4 days; sequelae, icp pressure bolt and management - mannitol

🗑

Acute Bacterial Meningitis Prevention

HIB; N. Mening multival poly cap vacc ACY and W-135 not B(U.S) - effect in 3mo up; pneumovax: 23 poly caps(the majority of ABM) - adults>65; chronic disease; DM; EtOHism; CSF leak; immunocomp;asplenia, lymphoma, HIV neph synd or multi myeloma 6mo boost

🗑

Acute Bacterial Meningitis phrophylaxis

menigoccal disease: rifampin, monocycline, cipro; Hflu rifampin

🗑

Stretch Reflex(myoactic, deep tendon)

Stimulus: stretch of the muscle SAR: Muscle spindle to the chord; MER: AMN(Extrafusal fibers) contracts muscle, GMN contracts the muscle spindle(intrafusal)

🗑

Muscle Spindle

afferent to the cerebellum, Nuclear bag, annulospiral endings detect length and rate of change, Nuclear chain has flowerspray endings and detects change in length

🗑

upper arm(lateral surface) chord segment

🗑

Thumb and lateral forearm cord segment

🗑

middle finger cord segment

🗑

little finger cord segment

🗑

nipple cord segment

🗑

Umbilicus cord segment

T10

🗑

Big toe cord segment

🗑

Heel cord segment

🗑

Elbow flexion cord segment

🗑

Elbow extension cord segment

🗑

Wrist flexion cord segment

🗑

Wrist extension cord segment

C6, C7

🗑

Knee Flexion cord segment

L5, S1

🗑

Knee extension cord segment

L3, L4

🗑

Ankle Dorsiflecion cord segment

🗑

Plantar flexion cord segment

🗑

Withdrawl reflex

Stim: pain. Sensory afferent, motor efferent flexors excited, extensors inhibited

🗑

Reflex scale

0-areflexia. 1-hypo, 2-normal, 3 hyper, 4-clonus(spinal cord severed)

🗑

Crossed Extensor Reflex

Stimulus: pain on opposite side, sensory afferent, motor afferent flexors inhibited extensors excited; usually linked with withdrawl

🗑

Noiciception

recognition and signaling of a deleterious stimuli

🗑

Pain

conscious awareness of the nociceptive event

🗑

Suffering

emotional and behavioral sequelae

🗑

Deafferention pain

pain due to loss of sensation of an afferent fiber

🗑

Hyperalgesia

increased sensitivity to stimuli

🗑

Pain afferent nerve ending activators

thermal, mechanical, chemical(H+, bradykinin, histmaine, prostaglandins, hypoxia)

🗑

A-delta Fibers

location: body surface/skin, Stimuli: mech, therm, and chem. type of pain: sharp prickly pain, large diamerter myelinated 5-30m/sec

🗑

C fibers

Location: deep skin and all tissues; Stim: therm, mech, and chem, type of pain: aching, burning pain, small diameter unmyelinated .5-2m sec

🗑

Lissares tract

afferent pain neurons synapse with spinal chord and decusate at two spots, one at the level and one 2 segments above(lissares) using substance P and glutamate

🗑

Cord damage to one side

no pain contralateral side 2 segments down because of lissares

🗑

Neospinothalmic tract

Ascending pathways of pain Lateral spinothalamic tract: 1. RAS 2. Thalamus(VPL) 3. Somatosensory cortex; does paon localization and intesity; a delta uses this the most

🗑

Paleospinothalmic Tract

Ascending pathways of pain Lateral spinothalamic tract:1. RAS 2. thalmus(VPL), 3. intralaminar nuclei 4a. Somatosensory cortex(secondary/how er interpret pain) 4b. limbic(prefrontrontal cortex); emotinal response to pain

🗑

Modulation of pain

1. periaqueductal gray releases enkephalin on internneruon that releases neurotensin on the 2. Raphe nucleus(medulla)which releases 5HT on a interneuron which releasts enkephalin on the 2. opiod recptors of the dorsal horn which stops ca++ channels

🗑

Epidural

phentyl(100x morphine/antidote naicam) binds opoid receptor in dorsal horn stops Ca++ channels

🗑

Tricyclic Antidepressants and pain modulation

Block reuptake of 5HT, NE, and DA; more 5Ht in the CNS more ENK less pain; SSRI don't cross BBB

🗑

Exogenous modulation of pain - opiates

oral/iv/im(euphoria); Epistays local no euphoria; intrathecal(subarachnoid space spreads with CSF movement)

🗑

Exogenous modulation of pain - local anesthetic agents

Lidocaine(short)MSD:5-7 mg/kg, tox: cns before cardiac, CNS: twitch tinnitis, GM seiz, card: heart block; Marcaine(long) MSD: 2-3mg/kg, toc cardiac(DIC) before CNS(V. Fib); Nsaids(block prosta; tricyclics

🗑

Surgical Modulation of Pain

Cordotomy: lateral spinothalmic tractotomy, loss of pain on contra side 1-2 seg below, temp.(reroute) SE:no cerebellar input/loss of balance; Lesions-dermato pain(shingles), rhixotomy, intralamin nuclei obliterate(no suffering just acute pain); VPL or VPM

🗑

Radicular Pain

Follows dermatome

🗑

Thalamic syndrome

vascular lesion, hypoxia to thalmus often VPL

🗑

Complex regional pain syndrome(reflex sympathetic dystrophy) - component 1

1.pain: out of prop to injury, burn, numb ting, itch, derma(vasc. dist) or diffuse(less), distal, super nonocious stim(air hurts, behavioral changes(reclusive or withdrawn)

🗑

Complex regional pain syndrome(reflex sympathetic dystrophy) - component 2

unspecified abnormalities of sensation, motor function and blood flow: bad cap refill, soft puffy edema, color changes, cold or warm, joint limitations

🗑

Complex regional pain syndrome(reflex sympathetic dystrophy) - component 3

Sweating and trophic changes in the skin and soft tissue: excess moisture or dryness, increased haro or nail growthm osteoprosis(affected area), muscle atrophy

🗑

Complex regional pain syndrome(reflex sympathetic dystrophy) - 3 types

algodystrophy: pain and all features of dystrophy; dystrophy without pain; sympathetically maintained pain, not exhibiting dystrophic changes

🗑

Complex regional pain syndrome(reflex sympathetic dystrophy) - treatment

meds: phoxybenzamine hydrochloride(alpha blocker), clonidine(alpha 2 agonist(blocks symp at synaptic cleft) all meds have postural hypotension; Nerve blocks(first and fast) inject into dorsal root ganglion; cut the nerve

🗑

Crude touch

same side; anteriolateral system

🗑

Discriminatory touch(conscious proprioceptive)

ascends same side in fasiculus gracilus decusates in nucleos gracilla(medulla) goes to SS cortex

🗑

Myopathy

proximal: going up stares; CPK; EMG;

🗑

Neuropathy

Distal:button shirt, gradual, painless

🗑

Lesion in the anterior horn

volunt motor control: pralysis(flaccid, hypotonia; Reflex motor: decreased/absent, atrophy: profound, Fascic: motor unit(see), Fibril:fiber(emg)

🗑

Posterior Root Lesion

causes: tumor, infection, injury(IVD hern); Manifests: dermatomal/radiculopathy; motor volunt motor: ok/uncoordinated(no cerebellar sense); atrohy/fascic:absent; hypotonia; sensory: pain, paraesthesa(sciatica); reflexes decreased or absent.

🗑

Upper motor Neuron Lesions: internal capsule(posterior limb) - intial

manifests:(7-21d, shock like, paralysis: contra, flaccid, hypotnia, Refelxes: DTR-absent, Babinksi-no response

🗑

Upper motor Neuron Lesions: internal capsule(posterior limb) - long term

Manifests: paralysis: contr, spastic, hypertonia: flexors of arm, extensors of legs(fetal posit), reflex: DTR:4+, Babinski + on contra, hoffman normal: hyperreflexive

🗑

Upper motor Neuron Lesions: Corticospinal lesion

Above decusast: contra, spastic paralysis, babinski: +; Below: ipsi, spastic paralysis, babinski:+

🗑

Lesions of peripheral Nerves: Mononeuropathy

1 nerve, cause:trauma, entrampment(IVD), infection, vascular, pain common

🗑

Lesions of Peripheral Nerves: Mononeuropathy multiplex

asym, 2 or more, more proximal, prevelent in autoimmune or DM before they go poly

🗑

Lesions of Peripheral Nerves: polyneuropathy

generalized, Motor: sym, distal the proximal, weak, atrophy; Sensory: stocking and gloves appearance(feet before hands, upper calf before fingers); Reflex:absent or dec; ANS: dec. sweating, bladder/bowl, blood pressure, sexy dysfx

🗑

Lesions of Peripheral Nerves:plexopathy

Nerve plexus incolved, trauma, tumor, infection, compression, Erb's palsy: usually upper trunk of brachial(c5-t1) to much force during delivery, shorter arem from disuse

🗑

Lesions of Peripheral Nerves:Amyotrophy

muscle atrophy secondary to damaged nerve

🗑

Lesions of Peripheral Nerves:myopathy

weakness due to a problem with the muscle

🗑

Lesions of Peripheral Nerves:myositis

muscle destruction, inflam, immune

🗑

Lesions of Peripheral Nerves: sensory deficits

Large fibers: pins and needles, small fibers: decrease in pain and touch, Hypesthia-dec/alt sensitivity, paraesthesia-pins and needles, dysesthesia-bad pain, hyperesthesia-inc repsonse to pain

🗑

Lesions of Peripheral Nerves: polyneuropathy causes

DANG THE RAPIDST:DM, EtOH, Nut(B12, Thiamine), GBS, Trauma, Hereditary, Enviro(acrylamide, lead, arsenic, remote effects of cancer, amyloid, porphyria, inflan/infect(vascular), syph/systemic(hypothryoid), tumor

🗑

Diabetic Neuropathy

most com cause of polyneur, based on duration and severity, slow insidious with minimal motor, normal polyneuro pres, proprio: dec joint posit leads to destruc(diabetic pseudo tabes), DM amyotrophy-weak,atrophy in prox mm, lumbosac polyrad(L2-4)

🗑

Peripheral nerve testing

Nerve conduction velocity, EMG, F wave: conduction velocity in proximal nerve and nerve root, H wave: reflex arc.

🗑

GBS(acute Demyelinating Inflammatory Polyneuropathy)

Causes: post infection viral(CMV, EBV), progressive weakness in >1limb with areflex or hypo; Pathology: demyel over 1-3 weeks; Sensory may be 1st follow by ascending m weak, motor:distal b4 prox, Leg b4 arm; CNs, ANS:arryth, bladderm tenp, fluctuating bp

🗑

GBS(acute Demyelinating Inflammatory Polyneuropathy) - Diagnosis + treatment

Dx: CSF: inc protein, emg prolonged F wave and no H wave; Tx:steroids:contro, vent, plasmapharesis, ig

🗑

C5-C6 IVD herniation

C6 root compression; Sensory Dec over thumb lateral radius, Motor weak elbow/flexion/bicep; Reflex: dec bicep/bracioradialis

🗑

C6-C7 IVD herniation

C7 root compression; Sensory Dec over index and missle digit, Motor weak elbow/extension/tri; Reflex: dec tri

🗑

L4-L5 IVD herniation

L5 root compression; Sensory: dec. over anterolateral big toe; Motor: weak dorsiflexion(heel walking); Reflex: dec hamstring

🗑

L5-S1 IVD herniation

S1 root compression; Sensory: dec. over lateral leg and heel; Motor: weak plantarflexion(toe walking); Reflex: dec ankle

🗑

IVD herniation diagnosis and treatment

MRI, Myelogram(young and healthy; conservative: PT, corito inject; Surgery if motor def.:laminectomy with repair or fusion

🗑

Spinal cord Injury Statiitics

10k/year, 50% quads 50% para; 81% males 34y, common locations c1-2, c4-7 T-L2; causes: 48% MVA, 21% falls, 14.6% trauma, 14% sports(water)

🗑

Types of Spinal Cord Injuries

compression, extension, flexion, rotational, lateral

🗑

Spinal cord injury classification ASIA

Based on neuro levels, touch and prick each derma, and strength of: shoulder shrug(c4), elbow flex(c5), wrist flex(C6), Elbow ext(C7), hip Flex(L2); A:complete loss, B: incomp, some sensory, C:incomp some motor pres<.5, D incomp, .5 muscle pres, E:normal

🗑

Spinal cord injury - immediate

submicroscopic hemorrhage->edem+/- 2 segments, neurogenic shock(hypotension, bradycardia, hypothermia, tx fluids, vasopressor), spinal shock

🗑

Spinal Shock - Spinal cord injury

7-21day, absent reflexes, flaccid paralysis, no sensory or ANS(over distended bladderimpacted rectum) babinksi absent

🗑

Spinal cord injury - long term

return of spinal cord reflexes, dependent on level of injury, autonomic hyper-relfexia

🗑

Autonomic Hyper-reflexia

Massive rerouting through the sympathetic trunk, bladder distention can activate it. below T6 you don't have enough space to hold the blood displaced by the vascon, TX alpha blockers(postural hypotension, pooping schedules and dialy straight caths

🗑

Review the information in the table. When you are ready to quiz yourself you can hide individual columns or the entire table. Then you can click on the empty cells to reveal the answer. Try to recall what will be displayed before clicking the empty cell.

To hide a column, click on the column name.

To hide the entire table, click on the "Hide All" button.

You may also shuffle the rows of the table by clicking on the "Shuffle" button.

Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.

Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

Normal Size Small Size show me how

Created by: bmg4