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60 Cards in this Set

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VIGNETTE 1

A 38 year old man is found unconscious in a downtown dumpster. During transfer to the ER he transiently regains consciousness, but then lapses into deep coma. On exam in the ER, his neck is stiff and his temperature is 103 F. There is alcohol on his breath, and his liver is 6 inches below the costal margin. Needle track marks are noted on both arms. He is unresponsive to verbal commands but is breathing spontaneously and withdraws to painful stimulation. The withdrawl is much less vigorous when the left hand or foot is stimulated, and muscle tone and reflexes are increased on the left.

(1) What is coma?

astate of consciousness in which there is lack of both wakefulness and awareness. “unarousableunresponsiveness”

(1) What is the DDX of coma?

1. Brain death- permanent absence of cerebral AND cortical functions


2. Locked insyndrome- limb paralysis, no speechwith retained consciousness, alertness, cognition


3. Persistentvegetative state- WAKEFULNESS withoutawareness (presence of sleep-wake cycles)


4. Frontal lobedisease-prefrontal and bilaterallesions


5.Nonconvulsivestatus epilepticus- complex partialand absence seizures


6. Psychiatricdisorders- pseudocoma, depression,catatonia

(1) What are etiologies of coma states?

alcohol/drug overdose, herniation syndrome, metabolic coma (hyper/hypo glycemia, thyroid, uremia), brain stem lesion, akinetic mutism, catatonia, stroke, acute intercranial hemorrhage, brain abscess, brain tumor, anoxic injury, hypo/hyperthermia.

(1) How can you localize the lesion of a coma state?

supratentorial- damage to white matter tracts from midbrain tocortex –think decorticate posturing


infratentorial- damage to brainstem, reticular activating system lesions- think decerebrate posturing, respiratorydisturbance, pupillary abnormalities


systemic- no focal signs, abnormalities are symmetric. Acute confusional state precedes coma.

(1) How would you evaluate a coma patient?

1. history: anywitness


2. physical exam: skin, temp, breath, bp, cardio, abd, neuro-GCS,Kernig, Brudinski signs, pupillary response, ocular motility, corneal response,motor response, respiratory patterns 3. Labs: blood and urine drugand tox screen-sedative drugs and alcohol; CBC, UA, Chem, ABG, blood cultures (fever)


4. Other: ECG forarrhythmias; CT or MRI if structural lesion is suspected (CT without contrastis quick and can ID hemorrhages); LP for meningitis, EEG for seizure disorders

(1) How would you treat this coma patient?

-stabilize pt’s ABCs, intubation depending on clinical picture


-dextrose, thiamine, naloxone for possible overdose


-empiric antibiotic and antiviral therapy for suspected baterial meningitis or viral encephalitis


-neurosurgery for some causes of structural coma

VIGNETTE 2

A 68 year old retired career military veteran presents with a 3 year history of progressive memory difficulty. Past medical history is remarkable for repeated episodes of closed head injury with loss of consciousness, heavy alcohol abuse, 60 pack year smoking history, and a 20 year history of poorly controlled hypertension. Family history is remarkable for the patient's mother who died at 75 years of age, after a prolonged cognitive decline. Medications include aldomet, tagamet, and 50mg of benedryl for sleep. He complained of feeling sad, with low energy level, poor sleep, and anorexia with a 30 lb. weight loss. Physical exam reveals a BP of 190/95 and bilateral carotid bruits. The patient is alert and oriented to person and place but gives the year as 1972. Remote memory is good, but he could not recall any of 3 objects at 5 minutes. He made several paraphasic errors in spontaneous speech. No neglect is present. Moderate visual-spatial difficulties are noted on copying and drawing. The remainder of the exam is normal, except for a stiff gait with small, shuffling steps (marche a petit pas) and a left babinski sign.

(2) What is dementia? Ddx?

dementia = decline in memory + cognitive function or executive function.


1. degenerative: Alzheimer’s,Parkinson’s, Pick’s, Lewy body, Huntington's


2. vascular (multiple infarcts, stroke, vasculitis) 3. infections (meningitis, HIV, encephalitis, syphilis, CJ disease)


4. psych (eg depression, EtOH abuse)


5. toxic/metabolic (B12. Hypothyroidism, heavy metals, toxins)


6. tramatic (subdural, head injury, anoxic injury)


7. tumor (glioblastoma, lymphoma, mets)

(2) What is the most likely causes for dementia in this patient?

Most likely = Alzheimer’s –> family history of cognitive decline progressive over several years (cognitive decline with Alzheimer’s begins and progresses insidiously)


Other = vascular (risk factors = HTN, smoking, signs of cardiovasculardisease, focal neuro deficits), Parkinson's (slow/shuffling gait), chronic traumatic encephalopathy (hx of repeat injury

(2) How would you evaluate a patient with dementia?

history: get collateral from others (patientdifficulties, time course, functioning of patient, safety issues, etiologic hx,family hx)


physical: more detailed neuropsych testing, start w/Folstein MME


labs: CBC, lipid panel, B12/folate, LFT’s (ammonia), BMP, HIV test, RPR, TSH.


other: CT or MRI

(2) Treatment for a patient with dementia?

Alzheimer's: options for meds are acetylcholinesterase inhibitors or NMDA receptor agonists. Psychosocial intervention for behaviors. May need anti-psychotics (atypical) for behavioral disturbance.


Vascular dementia: treatment consists of anti-hypertensives, anti-coagulation w/aspirin or wafarin (based on CHADS2 score)

VIGNETTE 3

A 24 year old man presents to the ER witha single generalized tonic-clonic seizure. His medical history is significantfor febrile seizures as a child and a remote history of head injury with lossof consciousness following a motor vehicle accident. He has a history of asthmafor which he takes theophylline. He admits to sleep deprivation, "pullingtwo all-nighters" to study for final exams. His family history is positivefor a brother and two cousins with epilepsy. His neurological exam is normal, but urinetoxin screen reveals cocaine metabolites.

(3) What is seizure and ddx?

Seizures = sudden change in behavior that is the consequence of brain dysfunction. Epileptic =abnormal neuronal activity, provoked seizure = metabolic derangement, drug/alcohol withdrawal, stroke/encephalitis.


DDX: epilepsy, pseudo seizure, syncope, TIA, panic attack, drug intoxication, drug withdrawal, malingering, migraine, sleep disorder, theophylline toxicity, movement disorder, hypoglycemia

(3) How would you evaluate a pt with seizure?

1. history: circumstances leading up to seizure (including aura),ictal behavior, postictal state, seizure triggers, prior seizures (including febrile seizures in infancy), prior response to anticonvulsants, witnesses


2. physical: lookfor focal neuro deficits, evidence of tongue biting


3. labs: electrolytes, glucose, calcium, magnesium, hematology studies, renal function tests, liver function tests, and toxicology screens


4. other: EKG +-/ holter monitor (if syncope likely), MRI (exclude structural abnormality), EEG, +/- LP

(3) Whatis the difference between seizure and epilepsy?

Epilepsy = recurrentepileptic seizures due to a geneticallydetermined or acquired braindisorder. Not due to infection, drug withdrawal, acute metabolicchange or fever cause = hyper synchronization of neuronal networks incerebral cortex


Seizures = suddenchange in behavior that is result of brain dysfunction. Non-epileptic seizures = non-recurrent and provoked, in setting ofmetabolic derangement, drug/alcohol withdrawal, acute stroke. Not associated with typical neurophysiologic changesassociated with epilepsy.

(3) Wouldyou treat this patient with anticonvulsants?

No, he cannot yet be diagnosed with epilepsy and there are multiple risk factors that confounds ability to say this was “unprovoked”. Risk factors include cocaine toxicity, recent sleep deprivation, side effects of theophylline. Should only start AEDs if diagnosis of epilepsy is well-established (ie knowthat seizures not provoked). Even though familyhistory and childhood hx of febrile seizures do point to possibility ofepilepsy.

VIGNETTE 4

A 72 year old man presents for evaluation oftremor. His wife has noted that he has "slowed down" over the lastseveral years, with particular slowness in movements. He has noted difficultywith his handwriting, and is aware of mild drooling. The tremor occurspredominantly at rest, but persists during activity, intensifies during timesof anxiety or fatigue, and resolves during sleep.His medical history is significantfor GE reflux, for which he takes reglan. His doctor started him on Mellarilfor a sleep disturbance. Family history is negative, but the patient thinks hismother and grandmother may have had a tremor. Exam showed a masked facies with diminishedblink rate and slight drooling. Mental function was normal. Eye movements werefull. Strength and sensation was intact, but tone was increased in alldirections of movement, with slowness and stiffness of movement. There was a 5Hz "pill-rolling" tremor at rest, which diminshed slightly withmovement. He ambulated in short, shuffling steps and turned en bloc with mildretropulsion.

(4) What is the differential diagnosis of Parkinson's?

Parkinson’s disease, essential tremor, drug induced movement disorder (reglan), tardive dyskenesia, Parkinson-like disorder, other neurodegenerative disease (Huntington’s,Frontotemporal dementia, Lewy Body dementia)

What is the likely pathophysiology of


Parkinson's and what anatomic structures are involved?

Basal ganglia dysfunction, lossof dopaminergic neurons in substantia nigra. Also get Lewy-Body formation.

How would you treat a patient with Parkinson's?

Change his current medications (reglan and mellaril) as both as dopamine blocking agent and have the potential to worsen his extra-pyramidal symptoms. He is not presenting at an early stage, start him on l-dopa + carbidopa and perhaps a dopamine agonist such as ropinirole. Other medication options include amantadine (bradykinesia, rigidity, gait disturbance) or MAO inhibitors to enhance l-dopa’s effects. Deep brain stimulation would be premature at this time.

VIGNETTE 5

A 35 year old woman presents forevaluation of headache. She was lifting a 50 lb box when she developed thesudden onset of "the worst headache of my life". She dropped to theground and transiently lost consciousness, vomitted, and was brought to the ER. She has a long history of "sickheadaches" which are similar to the current headache, though generallyless severe. On several occasions, she developed visual loss off to the rightside for 15 minutes, often followed by left arm and face tingling, whichtypically preceded the onset of the headache. She smokes 2 packs/day and takesOCP. Her mother and sister both suffer from headaches. Exam showed an ill-appearing women lyingon a stretcher with the lights off. She complained of photophobia, and her neckwas stiff to passive movement. Fundoscopic exam was difficult, but the internthough he saw bilateral pre-retinal hemmorhages. Her neurological exam wasotherwise normal.

(5) features of SAH? DDX?

features: sudden-onsetsevere headache associated with loss of consciousness, N/V, menigismus, pre retinal hemorrhage


DDX: migraine (headache, photophobia, vomiting, h/o OCP use), cluster headache, meningitis, pseudotumor cerebri, TIA, seizure, tumor, tension headache

(5) How would you evaluate a pt with SAH?

History: previous headache, age of onset, characteristics, associated symptoms, family history


PE: basic neuro exam


Labs: CBC, chemistries, ESR/CRP, PT/PTT, thyroid, ABG, tox screen, UA


Imaging: For SAH: noncon CT -> LP (even if CT neg) -> urgent four-vessel angiography (to detect intracranial aneurysms) or MRA

(5) What is the treatment for SAH?

- Neurosurg consult


- Admit to ICU for continuous hemodynamic and neuro monitoring. Initial tx = bedrest, analgesia, compression stockings, d/c antithrombotics. Lower bp with IV beta blockers, nimodipine to prevent vasospasm. Consider prophylactic antiepileptic drug therapy.


-surgical: surgicalaneurysmal clipping and endovascular coiling = effective in preventingrebleeding and generally should be performed early



(5) Whatare the diagnostic criteria for migraine?

> 5 attacks that lasted 4-72 hours


-at least 2 of the following :(unilateral, pulsating, moderate-severe pain, worse with physical activity)


-at least 1 of the following -> nausea/vomiting or photophobia and phonophobia

(5) What are the different treatments for migraine?

reduce triggers: lack of sleep,foods, stress.


non-pharm: biofeedback, CBT, relaxation therapy, occipital nerve stimulators.


abortive: analgesics (nsaids, acetminophen, fioricet) anti-nausea. ergotamine (vasoconstrictor – for severe migraines), sumatriptan (5HT agonist – don’t give to pts with known CAD), IV metoclopramide.


prophylactic: TCA, beta blocker, valproic acid, topiramate, botulinum toxin

VIGNETTE 6

A 52 year old man developed back painafter a motor vehicle accident. Over the course of the week, his pain worsenedand radiated down to his right foot and great toe. He had difficulty walking,noting that his right foot would slap on the ground. Pain was better lying onhis left side with his knees slightly bent, and was worsened in the sittingposition. His history was significantfor multiple prior back injuries. Exam showed a positive straight leg raiseat 30 degrees on the right and 60 degrees on the left, with worsening pain downthe right leg. He was unable to bend forward beyond 30 degrees. There wasmoderate weakness of right foot dorsiflexion, eversion, and inversion. Hipextension and knee flexion were normal. Sensation was diminished over the rightgreat toe, dorsum of the foot, and lateral leg. Reflexes were normal.

(6) Localize the lesion. Other locations in CNS/PNS?

Motor sx's: R great toe = L5 , Foot dorsiflexion/inversion = L4 Foot plantarflexion/inversion = S1.


sensory sx's: sensation decreased in right great toe, dorseum of foot, lateral leg = L5-S. Given the + straight leg raise, suspect nerve root injury.


Other: lumbrosacralsprain, arthritis, fracture, metastatic disease, bone tumor, diskitis, epiduralabscess, ankylosing spondylitis, tethered spinal cord, spondylolisthesis,paget’s disease, peripheral vascular disease.

(6) clinical features of low back musculoskeletal sprain

presents with deep/superficial ache, throbbing, burning or tenderness, diffuse or local. Associated with paravertebral muscle spasms, stiffness, decreased ROM. No red flags (night pain, fever, leg pain, weakness, numbness, bladder/bowel dysfunction, major trauma or spasms, weight loss, lethargy, hx of infection, IV drug use, carcinoma, legal claims). Straight leg raise causes back pain only. Etiology includes arthritis, myopathies, trauma.

(6) clinical features of unilaterallumbar radiculopathy

Abnormality at the level of nerve root, usually affects single spinal level, often result of disk compression 90% L4-L5, L5-S1. May also be due to non compressive etiology such as inflammation, infection, neoplasm, vascular. P/w back and leg pain, burning, numbness and tingling in toes. Straight leg raise positive. L5 radiculopathy = back pain radiating down lateral leg S1 radiculopathy = back pain radiating down posterior leg. Weakness of foot dorsiflexion, eversion, inversion, toe extension, decreased sensation in first web space and over dorsum of foot, normal reflexes.

(6) clinical features of lumbar stenosis

Narrowingof the spinal canal, most commonly due to degenerative osteoarthritis. Causes mechanical compression of nerve or vascular supply. P/w “neurogenic claudication”, lower extremity discomfort, weakness, sensory loss. Usually6th decade or older. Pain is producedor exacerbated by walking or prolongedstanding, and improves with rest orforward bending. Tends to involve entire leg, not just one nerve distribution, usually bilateral.

(6) clinical features of conus modularis / cauda equina syndrome

Spinal cord ends at L1-L2. Distal part of the cord = conus medullaris. Caudaequina syndrome affects lumbosacral nerve roots below the cord. Bothsyndromes cause disturbances in bladder and bowel function (retention), backpain, saddle anesthesia, weakness of leg muscles. Cauda equina = LMN sx only, conus medullaris = UMN and LMN signs (bc spinal cord affected).

(6) therapy for lumbar radiculopathy

avoid provocative activities, acetaminophen/NSAIDS, short course opioids for severe pain only, physical therapy, muscle relaxants, heat, limit lifting. NO bed rest!


surgery (discectomy) for persistent severe pain with evidence of herniation and compression

VIGNETTE 7

A 32 year old woman acutely developed afebrile illness with nausea, vomitting, and transient diarrhea lasting oneweek. Eleven days following her gastrointestinal disorder, she developednumbness and tingling in both feet. Her sensory symptoms progressed overseveral days, accompanied by weakness of both hands and unsteady gait. On admission she had sinus tachycardia,bifacial weakness, distal>proximal quadriparesis, generalized areflexia, andmarked vibratory and position sense loss in the feet>hands. Over the nexttwelve hours she developed dyspnea, air hunger, and ventilatory failure.

(7) What is the DDX of acute, progressive generalized weakness?

Anteriorhorn cells: poliomyelitis


Polyradiculoneuropathy:GBS·


Acuteneuropathy: GBS, lyme, HIV, heavymetals· Neuromuscularjunction: botulism (inhibits Ach release), tick paralysis, organophosphatepoisoning, myasthenia gravis

(7) Whatis the anatomical localization and pathophysiology of Guillain-Barre?

Guillain-Barre syndrome: acute inflammatory polyneuropathy


Pathophys: Immune mediated, due to molecular mimicry. Immune response can be directed towards myelin or axon of peripheral nerve. H/o respiratory tract or GI infxn (campylobacter). Other triggering events = surgery, trauma, bone marrow transplant.


Sx's: progressivemuscle weakness and areflexia, with spontaneous remission

(7) How would you evaluate a patient with GBS?

Clinical presentation: progressive muscle weakness, decreased DTRs


Confirmatory tests = CSF (albuminocytologic dissociation – elevated protein, normal CSF WBC count), EMG (shows slowed conduction), Stool and serum antibodies to C. jejuni.

(7) How would you manage a GBS patient?

1. Supportivecare: critical bc high risk ofneuromuscular respiratory failure requiring mechanical ventilation. Closerespiratory monitoring w/ frequentmeasurement of vital capacityo Cardiac andBP monitoring (Can get autonomicdysfx). Tx of pain, some need ICU for respiratory management, autonomicdysfx. 20/30/40 rule: need ICU and intubation if FVC<20,max insp pressure <30, max expiratory pressure <40 (high risk ofimpending respiratory failure)


2. Diseasemodifying treatment – shorten time toneurologic recovery. Plasma exchangeand IVIG = equally effective. No longer use corticosteroids.

VIGNETTE 8

A 72 year old man presents with rightsided weakness. He was well until the morning of admission, when he suddenlyslumped over at the kitchen table. His wife relates that he bumped his head ona door the night before admission, without loss of consciousness. Over the pastseveral months he complained of two episodes of transient right hand weaknessand a single episode of painless visual loss in the left eye for 2 minutes. Hismedical history is complicated by coronary artery disease, s/p MI x 2 with anejection fraction of 25% by echocardigram. He had a CABG and prosthetic valvereplacement 2 years ago and is on warfarin. He has atrial fibrillation, poorlycontrolled hypertension, and diabetes. On exam, BP was 210/105 with anirregularly irregular pulse. He had an ecchymotic area over the left frontalregion and a left carotid bruit. He was awake and could follow simple commandsbut had no speech output. His eyes were deviated to the left, but could crossthe midline with dolls head maneuver. He consistently did not blink to threaton the right side. There was severe right lower facial weakness and a flaccidright hemiparesis, hand>arm>leg. Sensation was difficult to test, but hewinced to painful stimulation on the left side but not the right. There was aright babinski sign. He vomited once in the ER, and was more difficult toarouse on repeat exam two hours later.

(8) Whatis the anatomical localization of this lesion?

Right hand weakness: left motor strip, left internal capsule, left corticospinal tract in brainstem


No speech output: Broca’s area (dominant frontal lobe)


Follows only simple commands: Wernicke’s area (dominant temporal lobe)


Left eye deviation, maintains VOR: left frontal eye field lesion


Not blinking to threat on right: lesion beyond optic chiasm on left (left optic tract, left LGN, left optic radiations)


right lower facial weakness: UMN lesion – left motor cortex, left internal capsule


flaccid right hemiparesis hand>arm>leg: left motor cortex, MCA territory


decreased pain sensation on right: left sensory strip, left spinothalamic tract


right Babinski: left upper motor neuron lesion (left motor strip, left corticospinal tract)


LEFT MCA

(8) What diagnostic possibilities explain the deficit?

Stroke has two major etiologies: ischemia (80%) and hemorrhage (20%). Ischemia may be thrombotic with local thrombus formation or embolic.


1. Risk factors for EMBOLIC stroke in this patient = prior history of TIA’s, low ejection fraction (predisposing to mural thrombi), prosthetic valve (a potential source of emboli), and atrial fibrillation (predisposing to clot formation in the atria).


2. Risk factors for hemorrhage stroke in this pt =HTN, age, Coumadin, trauma. Presentation of hemorrhagic stroke = signs of increased ICP (HA, N/V, and drowsiness from increased ICP)

(8) How would you work up a stroke patient?

First step =stabilize patient, ABCs, check serum glucose, coags


Emergent imagingto r/o hemorrhagic stroke· Further imaging(MRI) more sensitive for ischemia, imaging to look for carotid stenosis(MRA/CTA/ultrasound)


ECG to documentatrial fibrillation. · Echocardiographyto look for thrombi in the chambers.

(8) How would you treat an ischemic stroke patient?

ischemic:


-t-PA may be given if patient presents within 3-4.5 hoursof onset of symptoms and as long as the patient has no intracranial hemorrhage.


- ASA or other anti platelet medication


- Can start anticoagulation(warfarin) in patients with a fib after 24-48 hours


-Antihypertensives (with caution), onlyif the hypertension is extreme (>220 systolic, >120 diastolic), or if thepatient has another clear indication (eg CAD, heart failure).



(8) How would you treat a hemorrhagic stroke patient?

hemorrhagic: patient’s risk factors point to ischemia, hemorrhage seems more likely in this case with rapid progression of increased ICP (vomiting, stuporous).


i. Control of increased intracranial pressure – elevate head of bed to 30 degreees, hyperventilation, mannitol


ii. Surgery – evacuation of clot


iii. Control of hypertension – weight risks andbenefits (benefit = reduce further bleeding, risk = reduce cerebral perfusion)


iv. Reversal ofcoagulopathy (as from coumadin)

VIGNETTE 9

A 65 year old woman presents in youroffice for evaluation of back pain and leg weakness. She was well until 2months ago, when she noted slowly progressive, focal, mid-thoracic back pain.The pain became severe and constant, and typically worsened in the eveninghours, The patient complained that she could not find a comfortable positionand often slept in a semi-upright position in a recliner. Coughing increasesher discomfort. Over the last week, she noted stabbing pains that would"shoot" around her rib cage onto her chest associated with vagueparesthesias. Yesterday she had gait unsteadiness and vague leg weakness and asense that she could not fully empty her bladder. Her medical history wasremarkable for modified radical mastectomy 5 years ago. She smokes 3 packs/dayfor 30 years, and recently complained to her doctor about a persistent cough;he obtained a CXR which reportedly shows a "spot" which "mayneed to be further evaluated."Exam shows focal tenderness to spinepalpation at T-10. Mental status, cranial nerves, and upper extremity armstrength and sensation were normal. There was moderate weakness of theiliopsoas, hamstrings, and tibialis anterior bilaterally. Tone was slightlyincreased in both legs. Vibration was markedly diminished to the knees, andproprioception was impaired at the toes. Pin prick sensation was reduced inboth legs and extended to the umbilicus before abruptly normalizing. Reflexeswere pathologically brisk at the knees with bilateral ankle clonus. She wasable to ambulate independantly with a mildly spastic gait.

(9) Localizethe lesion.

Sensory level ontrunk = spinal cordlesion. clear pin-prick level at T10, focal tendernessto palpation at T10 suggests something outside the cord (extradural) pushing in. Clear involvementof all spinal cord tracts below this level dorsal column (posterior cord): vibration decreased to the knees, proprioceptiondecreased at the toes. Corticospinal tract (lateral cord): weakness of the iliopsoas, hamstrings, and tibialisant. Bilaterally spinothalamic tract (anterior cord): pin prick reduced in both legs to level of umbilicus. Evidence of UMN involvement: increased tone inlegs, pathologically brisk reflexes at the knees, bilateral ankle clonus,mildly spastic gait. Descending pathto bladder is in the sacral cord, sospinal injury can cause bowel/bladder incontinence.· Shooting pains inchest suggest nerve root involvement.

(9) DDx

Epidural extension of vertebral body mets from primary tumor elsewhere in body (breast, lung)


Spinal cord primary tumor- these occur in the white matter. Include ependymoma and glioblastoma. This is more likely to be the latter, as the former occurs in the low cord and is usually painless.


Epidural abscess


Hematoma


AVM of cord


Herniated disc: very uncommon at level of thoracic spine

(9) Whatdiagnostic tests you would obtain to evaluate this patient? Specificallydiscuss the variety of different tests available, their sensitivity andspecificity.

MRI of entire spine: gold standard to visualize extent of disease over whole cord: soft tissue, bone. You want a gado-enhanced, T2 weighted image. Most sensitive and specific. CT myelogram: CT with contrast injected into the CSF (if you don’t use contrast, then CT won’t show the spinal cord very well, as it is surrounded by bone) . Myelography provides a very detailed picture (myelogram) of the spinal cord, nerve roots, subarachnoid space and spinal column. A plain radiograph of the spine. You can see vertebral collapse or dislocation; it’s fairly sensitive but very non-specific. Ie good for bony abnormalities.

(9) Whatdifferent treatment modalties are available, and how would you treat thispatient? Discuss the specific role of surgery for this disorder.

Acutely: epidural tumor is a neurooncologic emergency!! Give high-dose dexamethasone immediately to decrease edema and cord compression.


Definitive therapy: Radiation therapy would be first line tx b/c it is minimally invasive and outcome is the same as with surgery. Do this right away.


Decompressive laminectomy: may help temporarily, but the tumor is usually in the vertebral body, not the neural arch, so it’s not a true solution. Anterior vertebral body resection.

VIGNETTE 10

A 60 year old man presents with legnumbness and imbalance. He first noted tingling and numbess in the soles of hisfeet 8 months ago, which has slowly progressed in intensity and spread to hisankles. He loses is balance when he washes his face or walks to the bathroomduring the night. Lately, he has trouble walking in open spaces and upstairs.He often finds his toes "catch" on sidewalks, carpets, and whenwalking upstairs. There is no associated pain and his upper extremities areunaffected. His medical history is significant forhypothyroidism and rheumatoid arthritis for 20 years for which he has been onintermittent steroids. Small cell carcinoma was treated with chemotherapy 2years ago. He had an antrectomy 10 years ago for peptic ulcer disease. Headmits to routinely having 1-2 martinis with dinner for years. There is nosignificant family history, though the patient remarks that his brother andfather have very high arches. Recently, he complained to his doctor ofexcessive thirst and frequent urination. Exam showed mild distal weakness of toeextensors. Proprioception was moderately impaired at the toes, and vibrationwas absent at the anlkes. Pin prick was impaired in a graduated fashionextending to the mid-calf. Knee and ankle reflexes were absent. He haddifficulty ambulating without using a cane; although there was no overt ataxia,he had a slightly widened base and was forced to look at his feet when hewalked. Romberg sign was present.

(10) Localize the lesion.

Polyneuropathy bc many peripheral nerves affected at same time, affecting sensory and motor fibers. loss of proprioception and vibration sense, +romberg = dorsal columnloss of pinprick sensation = spinothalamic tractmild weakness of toe extensors, absence of patellar reflex = corticospinal tract. Losses start at S1 and progress to L4-L5.


S1: numbness and tingling in soles of feet, absent ankle jerk


L5: decreased toe extension (toe extension)


L4: absent patellar reflex


L4-S1: decreased sensation to pin prick from toes to mid calf

(10) What are the most common causes of polyneuropathy?

diabetic neuropathy, hypothyroidism, nutritional deficiency (B12, B6, thiamine, vitamin E).


Toxins and medications: lead, isoniazid, chemotherapy (vincristine especially), aminoglycosides, ETOH


post-infectious/autoimmune: GBS, SLE, polyarteritis nodosa


Infectious: Lyme, diptheria, HIV, leprosy


other: small cell ca -> paraneoplastic syndrome

(10) How would you evaluate patient?

Electrolytes, esp. BUN and creatinine, also glu. 24-hour UA, B12, TSH, T3/T4; LFTs CBC- peripheral blood smear, MCV ESR, serum vitamin B12 CXR. STI testing.

VIGNETTE 11

A 25 year old nurse present with visualloss in her right eye. Last week she noted a mild ache above her eye, followedby a "scratchy" feeling when she would blink. The pain increased andwas worsened with eye movement. Two days ago her vision became blurry, colorsbecame "washed-out", bright lights were irritating, and acuity becameprogressively impaired. Six months ago she recalls a transient episode ofbladder incontinence. and 2 years ago she had numbness and tingling of herright leg for 3 weeks which resolved spontaneously. Her medical history isunremarkable, though she did have a URI 4 weeks ago. She asks if a vaccinationshe received 3 months ago could be related. Exam shows visual acuity of 20/100 O.D.and 20/20 O.S. Pupils were equal and reactive, but the swinging flashlight testshows a right afferent pupillary defect. Visual field testing showed a rightcentral scotoma with red color desaturation. Fundoscopic exam was normal. Therewas mild ataxia of the left hand on finger-to-nose testing. Pin prick wasdiminished on the right leg and extended up the right trunk to T4. There wasmild weakness and clumsiness of the left foot with left ankle clonus andbilateral babinski signs.

(11) What is the ddx for monocular vision loss?

vascular: retinal artery occlusion, retinal vein occlusion, TIA


trauma: corneal abrasion, foreign body


autoimmune: temporal arteritis, sjogrens, MS


neoplastic: retinoblastoma, opticneuroglioma


metabolic: complications from DM, hyperthyroidism


infectious: endopthalmitis (bacterial, fungal)


other: migraine headache, papilledema

(11) What anatomic structures are involved?

blurry vision: CN II (optic nerve),


bladder incontinence: S2,3,4


right afferent pupil defect: CN 2


ataxia of L hand onfinger-to-nose: R cerebellum


Bilateral Babinsk + ankle clonus – UMN involvement,otherwise non-specific


ataxia of L hand onfinger-to-nose – cerebellar dysfunction


diminished pin prick: left spinothalamic tract at level of T4

(11) How would you confirm the diagnosis of MS?

MRI showing periventricular demyelination, lesions greater than 0.6cm, lesions in posterior fossa


LP with CSF studies showing oligoclonal bands, increased IgG, may have increased protein, slight lymphocytosis


Evoked potentials studies

(11) What treatments are available for MS?

Disease-modifying therapy (for relapsing-remitting MS)


-interferon B


-glatiramir acetate


-IVIG


-teriflunamide


*Monoclonal antibodies effective but associated with significant adverse events: rituximab


Acute relapses: glucocorticoids, plasmapheresis


Symptomatic managment:pain control with pregabalin, gabapentin, amitriptyline, duloxetineexercise therapy, physical rehabilitation

VIGNETTE 12

You are called to evalaute a 78 year old man for confusion. He is post-op day #3 following CABG, and never appropriately awakened after surgery. The nurses report that his is constantly agitated, groping at his bedsheets, trying to get out of bed, screaming out but not making any sense, etc., and has received a variety of medicines to calm him down, including haldol, ativan, morphine, and bendryl. His blood pressure has been labile, recorded as low as 85/60, and his course has been complicated with CHF and pneumonia. He is also a diabetic, and was recently started on his miconase but has not yet started eating. His wife tells you that he has no prior history of confusional states, but has never before been hospitalized; he is a man of moderate temperment, who drinks alcohol with meals only. On exam, he is agitated and restless, frequently grabbing at bedsheets. His blood pressure is now 190/90, pulse 130, and he is diaphoretic. He is inattentive, disoriented, and will not follow any commands, His speech is slurred with prominent paraphasic errors, and he will not name or repeat. He would not cooperate will more formal mental status testing. His exam is otherwise nonfocal.