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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 C5
Thumb and lateral forearm cord segment C6
middle finger cord segment c7
little finger cord segment C8
nipple cord segment T4
Umbilicus cord segment T10
Big toe cord segment L5
Heel cord segment S1
Elbow flexion cord segment C6
Elbow extension cord segment C7
Wrist flexion cord segment C7
Wrist extension cord segment C6, C7
Knee Flexion cord segment L5, S1
Knee extension cord segment L3, L4
Ankle Dorsiflecion cord segment L4
Plantar flexion cord segment S1
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
Created by: bmg4