neuro Flashcards

1
Q

pathophys of stroke

A

-CVA -> is it venous or arterial
-Arterial:
-hemorrhagic or ischemic
-ischemic -> embolism, hypoperfusion (shock), thrombosis

-this is why shock can present with focal deficit

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2
Q

ischemic stroke (aka CVA)

A

-thrombosis or embolism
-2nd leading cause of death
-2nd MC disability
-MCC embolic- afib, thromboembolism
-RF- HTN, HLD, DM, smoking, TIA

-Negative sx and neuro deficits
-dysfunction is localized to brain area -> focal neuro deficit
-Onset- multiple sx (weakness AND sensory) occur simultaneously!
-thrombotic- gradual with stuttering pattern
-embolic or SAH- sudden and progressive

-weakness- raise arms 10s, pronator drift, weakness/paralysis
-CN- field cut, diplopia, blind, neglect (visual, sensory), pupillary size, EOM, expressive aphasia, receptive aphasia
-Reflex / cerebellar- finger to nose, heel to shin, reflex, babinski, gait

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3
Q

LVO syndromes

A

-Anterior cerebral artery (ACA)- contralateral WEAKNESS IN LEG > arm/face

-Middle cerebral artery (MCA)- contralateral WEAKNESS IN ARM/FACE > legs
-dominant side (MC left) = aphasia
-non-dominant side (MC right) = hemineglect

-Posterior circulation stroke-
-posterior cerebral, basilar, vertebral arteries
-dizzy/vertigo, ataxia, nausea, diplopia, dysarthria
-contralateral homonymous hemianopsia

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4
Q

POSTERIOR vascular territories

A

-Vertebral artery supplies brain stem and cerebellum
-Branches of vertebral artery: AICA, Basilar artery, PCA, PICA

-Crossed-findings are classic = Ipsilateral CN palsy + contralateral hemiplegia
-!5 D’s: dizziness (vertigo), dysarthria, dystaxia, diplopia, dysphagia
-!LOC, nausea/vomiting, ataxia, nystagmus are other common findings
-Require MRI for dx!!!!

-“Locked in syndrome”
-Basilar artery infarction
-Quadriplegia, can’t speak or swallow. Eyes are spared, and patients are awake and cognitively ware.

-Posterior inferior cerebellar artery (PICA) = Wallenberg’s syndrome
-Dysphagia, dysphonia are common
-Ipsilateral cranial nerve deficits with contralateral pain/temp loss
-Horner syndrome, Ataxia with a tendency to fall to affected side, nystagmus, vertigo can also be seen

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5
Q

wallenberg syndrome

A

-Lateral medullary infarct- Posterior inferior cerebellar artery syndrome (PICA) comes off vertebral artery​
-Dizziness, nystagmus, N/V, dysarthria, dysphagia, diplopia, hiccoughs​

-CROSSED findings​
-Ipsilateralfacial numbness (CN V)​
-IpsilateralHorner’s syndrome(sympathetic)​
-Ipsilateralgait ataxia (cerebellum)​
-Contralateralloss of pain & temperature sensation in limbs (spinothalamic)​

-Cerebellar findings on neuro exam:
dysmetria- failure of finger to nose

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6
Q

chart

A
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7
Q

alerted level of consciousness

A

-broad differentials
-if sus of stroke -> can be due to:
-increased ICP 2ndary to stroke- ICH, SAH, CVT, massive ischemic stroke
-large posterior circulation stroke
-thalamic or pontine hemorrhage

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8
Q

acute ischemic stroke diff dx

A

-hypoglycemia
-TIA
-hemorrhagic stroke
-epidural or subdural hematoma
-abscess of brain mass
-migraine
-todd’s post-ictal paralysis
-carotid or vertebral artery dissection
-cerebral venous sinus thrombosis

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9
Q

ischemic stroke presentation

A

-Ask amount of time passed since sx onset
-hx- family members or caregivers
-wake up stroke- last known normal = when they went to bed
-ask about cardiac hx, previous CVA, MI or TIAs, meds

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10
Q

door to needle time

A

-0 mins- suspected stroke arrives at ED

-<10 min- ABCs and POC glucose
-last known well
-exams

-<15 mins- notify stroke team

-<25- Head CT or MRI

-<45- interpretation of scan
-review eligability of tPA
-review labs

-<60- IV alteplase within 3-4.5 hours from sx onset

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11
Q

initial eval stroke

A

-AIRWAY:Can they clear oral secretions & maintain airway?
-BREATHING:Provide supplemental O2 if oxygen saturation is <94%
-CIRCULATION:Are they hemodynamically stable?
-Hypotensionwith evidence of poor perfusion (shock state) can mimic stroke especially in elderly patients and should be appropriately managed.
-Hypertension:Patients with cerebrovascular accidents frequently have high blood pressure. The approach to blood pressure management in ‘AIS’ is inherently different from the approach in acute hemorrhagic stroke. For this reason, a neuroimaging study (CT or MRI) is critical to help guide blood pressure therapy in patients with acute stroke.
-IV Access:Obtain peripheral intravenous (IV) access andavoid unnecessary lines, and ABGsince minor vascular trauma in patients with ischemic CVA who are deemed to be candidates for thrombolysis may become a real problem.
-Initiate labwork: Coagulation tests, CBC, BMP, lipid panel, A1C, T&S

-DISABILITY:Perform a focused neurological exam and obtain a point-of-care glucose!
-The focused exam is structured around relevant data gathered during the medical history and is catered to the differential diagnosis. The examiner should be focused on determining whether (1) there is a lesion and (2) where the lesion is localized.

-At the same time, neuro-stroke team should be called, and patient brought to the CT/MRI scanner, an IV is placed as labs are drawn, and pharmacy is alerted that tPA may be needed

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12
Q

NIH stroke scale and NINDS

A

-Quantitative measure of stroke-related neurologic deficit
-Must be uniformly administered each and every time!
-Important ideas:
-Administer scale items in their exact order
-Avoid coaching the patient
-Accept patients first effort
-Score only what the patient does (not what you think they can do!)
-Be consistent
-Include all deficits (even from previous strokes)

-1a – Level of Consciousness
-1b – LOC questions
-1c – LOC commands
-2 – Best gaze
-3 – Visual
-4 – Facial palsy
-5 – Motor arm
-6 – Motor leg
-7 – Limb ataxia
-8 – Sensory
-9 – Best language
-10 – Dysarthria
-11 – Extinction / inattention

-Each item is scored from 0 to a max of 4
0 = no deficit
4 = completely impaired
Highest possible score = 42
The higher the score, the worse the impairment

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13
Q

ischemic stroke: initial tests

A

-Non contrast CT head:
-Determines if hemorrhagic stroke
-Acutely ischemic zones are not usually visualized until 6-12 hrs after sxs

-If negative CT head
-Suggests an ischemic stroke
-Obtain immediate CTA head/neck for causative vascular lesions

-MRI / MRA head and neck
-Not routinely available
-Can detect earlier and smaller strokes
-Better for posterior strokes (vertebrobasilar, occipital, cerebellar strokes)

-ECG
-Look for atrial fibrillation . Large strokes may see deep TWI and prolong QT

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14
Q

ECG

A

-12-lead ECG of a pt with acute stroke, showing large deeply inverted T-waves.
-Large inverted T waves can be a sign of increased intracranial pressure (ICP) from ischemic stroke and edema, intracerebral hemorrhage etc.

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15
Q

If an older patient with multiple cardiovascular risk factors presents with new onset vertigo and a stroke is suspected, what is the best imaging modality?

A

MRI

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16
Q

ischemic stroke management

A

-Assess for reperfusion therapy with IV thrombolytic (tPA) within 60 min of arrival:
-Ischemic stroke diagnosis causing neurologic deficits that are not improving
-!< 3 hours since onset of symptoms (<4.5 in select individuals)
-!≥ 18 years of age
-See contraindications/precautions for tPA on next slide

-IV tPA dose:
-0.9 mg/kg, max dose 90mg
-Divided 10% as IV bolus over 1 minute, and 90% slow infusion over 60 minutes

-Dual anti-platelet therapy
-Minor strokes (NIHSS ≤5) do not always receive tPA
-Initiate DAPT within 24 hours of symptom onset
-ASA + clopidrogel/ticagrelor

-Endovascular therapy (EVT)/ Intra-arterial thrombectomy
-Embolectomy or angioplasty with catheters
-Indicated in LARGE VESSEL OCCLUSIONS! (LVO) in the ANTERIOR CIRCULATION!
-Can be done up to 24 hours! after symptom onset
-Can be done even if patient received tPA
-Indications:
-<6 hours from symptom onset (but up to 24 hrs)
-High baseline function prior to symptom onset
-Minimal tissue damage on CT
-NIHSS score > 6

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17
Q

tPA

A

-Absolute CI to thrombolytics:
-!Intracranial hemorrhage on CT
-Clinical presentation suggestive ofsubarachnoid hemorrhage
-!Neurosurgery,head trauma, or stroke in the previous 3 months
-Uncontrolled hypertension (SBP> 185mmHg or DBP >110mmHg)!
-!History ofintracranial hemorrhage
-Known intracranialarteriovenous malformation, neoplasm, or intracranialaneurysm
-!Active internal bleeding
-Suspected or confirmedendocarditis
-Knownbleeding diathesiswith platelet count < 100,000/μL
-Elevated PTT with heparin administered in the last 48 hours or with the use of oralanticoagulants
-Glucose< 50 mg/dL or >400mg/dL

-Relative CI:
-Recent GI orurinary tractbleeding (past 21 days)
-Minor or rapidly improving stroke symptoms
-Major surgery or serious nonhead trauma in the past 14 days
-Seizure at stroke onset
-Recent arterial puncture at a noncompressible site
-Recentlumbar puncture
-Post-MIpericarditis
-Pregnancy

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18
Q

thrombolytics complications

A

-Hemorrhage (intracerebral)
-Consider if: sudden neurologic deterioration, ↓ LOC, new headache, N/V, sudden rise in blood pressure
-STOP INFUSION
-STAT CT HEAD
-10U cryoprecipitate and 6U of platelets

-Hemorrhage (systemic)
-Minor bleeds do not require cessation: oozing from IV, ecchymosis, gum bleeding
-Major bleeds require cessation: GIB, GU bleed
-Seizure
-Angioedema (~2%)

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19
Q

increased ICP

A

-A deadly complication of intracranial bleeds and massive ischemic strokes

-New or worsening headache
-Altered level of consciousness
-Nausea vomiting
-Visual changes
-Papilledema
-Cushing’s reflex: Bradycardia, Hypertension, Abnormal respiratory pattern

-CT scan to look for cause and/or signs of ↑ICP (See Neuro 3 lecture)
-Management to decrease intracranial pressure
-Call neurosurgery and neuro ICU!

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20
Q

interventions to lower ICP

A
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21
Q

A 34-year-old male with no significant past medical history presents to the ED with worsening left sided neck pain, headache, ringing in his left ear, and his left eye looks more “droopy” than normal.
Symptoms occurred after riding on the “scariest rollercoaster” in the amusement park two days ago.
No other neuro symptoms
Vitals signs are stable
Neuro: GCS 15, A&Ox3
Left eye ptosis, miosis
Strength 5/5
Sensation intact
Normal gait, neg Romberg, Cerebellar intact
Neck: no ecchymosis, bruising, bruits, tenderness

A
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22
Q

cervical artery dissection

A

-MCC of stroke in people < 50 years old

-RFs:
-Any trauma (even minor, especially rotary) can stretch/torque the cervical artery
-Post-chiropracter manipulation, hair washing at salon, massage, shaving, swimming, coughing, sneezing, yoga, MVA
-Connective tissue disorder
-Migraines, Infections, OCP use, smoking, pregnancy post-partum

-Tear in the wall of the arterial wall
-Can lead to intramural hematomas and even emboli -> TIA/CVA symptoms
-sudden
-Sx can vary greatly depending on location
-!Head/face/jaw pain seen in 74%
-!Headache and/or neck pain 57-90%
-Horner’s syndrome 25% (just miosis/ptosis)
-CN palsy 8-16% (mostly CN 12,9)- rare
-Signs of ischemic stroke (weakness, numbness, vision changes)
-Pulsatile tinnitus 16-27%

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23
Q

cervical artery dissection: carotid artery dissection vs vertebral artery dissection

A

-Carotid artery dissection:
-Anterolateral aspect of the neck
-Radiates to jaw/face/head
-Neuro findings are often contralateral
-Partial Horner’s syndrome
-Cranial neuropathy 9 and 12 (contralateral)
-MCA/ACA stroke symptoms
-Transient monocular blindness (amaurosis fugax)
-Retinal artery occlusion

-Vertebral artery dissection:
-Unilateral, posterolateral neck and occiput
-Neuro findings can be contralateral or bilateral
-Posterior circulation stroke sxs
-Vertigo, diplopia, visual field deficits
-Wallenberg syndrome- Dysmetria, ataxia, ipsilateral hemiplegia, contralateral loss of pain and temperature sensation

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24
Q

cervical artery dissection: dx and tx

A

-Gold standard for imaging = digital subtraction angiography (rarely used)
-!!Because they tend to present as a stroke:
-!Will get a non con CT head first
-!Followed by a CTA neck ± MRA neck to determine the involved vessel

-Management of extracranial cervical artery dissections:
-Antiplatelet (ASA) or anticoagulation (LMWH)
-Consider endovascular stenting

-Intra-cranial do NOT get anticoagulated (no heparin/warfarin) due to risk of subarachnoid hemorrhage , can still get anti-platelets

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25
bells palsy
-Dysfunction of peripheral CN VII -#1 cause is HSV -Also consider Lyme disease, AOM, Tumor, HIV esp if bilateral -Acute onset (over hours) unilateral facial paralysis without forehead sparing! -CANNOT raise eyebrow on affected side -Drooping of the mouth -Incomplete closure of eyelids (can lead to exposure keratitis) -NO ROUTINE LAB OR DIAGNOSTIC TESTING -> CLINICAL DIAGNOSIS -Management: -Steroids: Prednisone 60-80mg qday x 1 week -Antivirals: Acyclovir or valacyclovir x 1 week -Antibiotics: If suspected or confirmed Lyme (doxy) -Recovery: 85% recover within 3 weeks -If red flags -> CT head non-con, CBC, CMP, Lyme titer, ESR, Thyroid panel
26
red flags of facial nerve palsy
-Cranial Nerve involvement other than CN VII -Bilateral facial palsy -Step-wise progression of facial palsy or slowly progressive beyond 72 hrs -Recurrent facial palsy -Prolonged facial palsy (>4 months) -Sudden-onset complete facial palsy -Weakness or numbness of arms or legs -Unaffected upper facial muscles (forehead) -Headache, visual deficits, nausea or vomiting -History of travel through woods or tick bite -Ulceration or blisters near ear -ramsay hunt syndrome- pic
27
primary headaches quick hits
-migraines: -Female, 10-30 yo, family history -Unilateral throbbing pain with photo/phono-phobia, nausea, vomiting -Triptans, NSAIDs are first line -cluster: -Unilateral lasting 30-90 minutes -Multiple headaches daily over several weeks (clustered) -No prodrome or aura, no N/V, no photo/phono-phobia -Signs: Ptosis, miosis, ipsilateral conjunctival injection, lacrimation, rhinorrhea -Tx: 100% O2 NRB 15 minutes and triptans -Tension: -Bilateral vice-like pain -No nausea/vomiting, photo/phono-phobia -Analgesics like Tylenol or NSAIDs -Other common causes: -Fever associated HA -Sinusitis -TMJ disease -Trigeminal neuralgia
28
cant miss HA
29
headaches in the ED
-98% of headaches have a benign cause -1% have an identifiable cause on their CT/MRI/LP -Meningitis -Hemorrhage -Hydrocephalus -Space occupying lesions -CVT -1% have headaches causes that cannot be ruled out on CT/LP alone -Cervical artery dissection (carotid, vertebral) -Cerebral venous thrombosis (CVT) -CO poisoning -Giant cell arteritis -Pre-eclampsia
30
red flags: SSNOOP4
Systemic symptoms (fever, weight loss) Secondary risk factors (HIV, cancer) Neurologic symptoms (confusion, impaired alertness) Onset: Sudden, abrupt, thunderclap Older: new onset or progressive over 50 years old (GCA) Previous headache: first time or change in pattern Papilledema Precipitated by exercise, position, Valsalva Pulsatile tinnitus -Subarachnoid hemorrhage Giant cell arteritis Post-lumbar puncture headache Infectious (meningitis, influenza) Cerebral venous thrombosis Idiopathic intracranial hypertension
31
PE for HA
-Observe -Migraines = vomiting, photo/phonophobia, avoidance of activity -Vesicular face -Autonomic activation (cluster) -Head / ENT -Temporal artery tenderness, pulses -Allodynia -Dental exam, sinus tenderness -Neck (meningeal signs, cervical dissection tenderness) -Eyes -Fundoscopy -Miosis, ptosis (Horner syndrome with carotid artery dissection) -Fixed dilated pupil (glaucoma) -Visual field cuts (PRES, pituitary apoplexy, migraine aura, occipital strokes) -Neuro exam!!!
32
primary headache management
-For those without red flags with severe headaches in the ER -1st line: IV antidopaminergics! as monotherapy -!Metoclopramide [Reglan] 10mg IV up to three doses -!Prochlorperazine [Compazine] 10 mg IV -!Droperidol [Inapsine] 5 mg IV -MC side effect: Akathisia!, administer diphenhydramine [Benadryl] if this occurs -Acetaminophen IV or PO, 325-1000 mg -Ketorolac 10-30 mg IV (30-60mg IM) -Triptans: -Mostly used in outpatient setting, less effective than IV antidoaminergics -Sumatriptan 6mg SQ once is recommended by the American Headache association -Contraindications to triptans include CV disease, uncontrolled HTN, pregnancy -Consider dexamethasone! 10 mg IV single dose to prevent recurrence 48-72 hrs post-ED discharge, if history of recurrent headache -Consider greater occipital nerve blocks
33
dystonic reaction
-Extrapyramidal effect after initiation of new drug -Painful, uncomfortable, but rarely life-threatening -IDIOSYNCRATIC (not dose related) -Most often from antiemetic or antipsychotic meds -Affects any striated muscle group: -Torticollar reaction -> twisted neck/face spasm -Buccolingual reaction -> protruding/pulling tongue -Oculogyric crisis -> deviated or roving gaze -Trismus -> difficulty opening jaw -Opithotonic -> spinal hyperextension -Management with anticholinergics! (benztropine, diphenhydramine) or benzos
34
headache lab tests
-Primary headaches don’t need lab tests! -If suspect temporal arteritis → ESR -If suspect meningitis → CSF studies -Cannot use CBC to rule-out meningitis -Add India Ink, cryptococcal antigen if suspect AIDS-related infection -If suspect CO poisoning → carboxyhemoglobin level
35
headache imaging
-Consider non-contrast head CT in patients with: -Thunderclap headache -Worst headache of life -Different headache from usual -Meningeal signs -Headache + intractable vomiting -New-onset headache in patients with: Age > 50yrs, Malignancy, uncontrolled HIV, Neurological deficits (other than migraine with aura) -Can rule out SAH for thunderclap headache if non-contrast head CT is negative and obtained within 6 hours of symptom onset. If further testing is needed after a negative head CT, can consider CTA, which is sensitive at detecting aneurysms >3mm versus LP based on shared decision making -Consider CTA head and neck for headaches associated with head/neck trauma or neuro deficits -Consider Brain MRI for red flag symptoms with a negative CT head -Consider MRV to evaluate for cerebral venous thrombosis for headache in the setting of hypercoagulability
36
temporal arteritis (Giant cell arteritis)
-Elderly patient with headache and temporal artery tenderness -Classic presentation: -Elderly person with gradual onset headache over weeks/months, jaw claudication, constitutional symptoms, low grade fever, with PMR symptoms, that progresses to visual loss -Strong associated with polymyalgia rheumatica! -Symmetric aching and stiffness of the shoulders, hip, neck, torse, worse in AM -!Diagnosis: ESR > 50mm/h, temporal artery biopsy -Treatment: High dose steroids! (do not wait for biopsy)
37
trigeminal neuralgia
-Episodic, sharp, electricity-like pain -Spontaneous remission -Can affect any trigeminal branch or more than one branch -Right > Left -M >F -Age: 50-60s -Treatment: Carbamazepine!!, baclofen, surgical decompression -Refer to neurologist for outpatient MRI -Sometimes associated with MS or intracranial lesion
38
idiopathic intracranial htn
-Previously called pseudotumor cerebrii -Young, obese female, hx of irregular menses -Common vitamin abnormality: Hypervitaminosis A -Chief complaint of headache (± blurry vision) -Insidious diffuse headache over days/weeks that is worse lying supine, waking in the morning, Valsalva -!!Nausea, vomiting, visual complaints, pulsatile tinnitus -cushing reflex = high ICP -> HTN, bradycardia, diminished respiratory effort -!!Dx: LP with high opening pressure >250mm CSF!! -PE: bilateral papilledema! -CT may show “slit like” ventricles -Tx: -Weight loss, acetazolamide, diuretics, therapeutic LPs, corticosteroids, shunt if necessary , neuro -Bad outcomes: blindness (peripheral -> central)
39
cerebral venous thrombosis (CVT)
-Very rare thrombosis of the brain – “DVT of the brain” -Females > Males, mean age of 39 years old -Common risk factors: -Hypercoaguable state (OCP use, malignancy) -Pregnancy and the peri-partum time -Local head/neck infection or injury -Clinical presentation varies widely, but almost always involves headache! -Typically the headache is gradual and progressive -Thunderclap -> think of associated subarachnoid hemorrhage -Progresses to focal neuro deficits, seizures, and decreased LOC -CT head is often performed first in an ER -30% of CT heads are normal, findings are usually non-specific -Small hemorrhagic lesions, vasogenic edema, venous infarction that does not respect the arterial boundaries, brain edema -CT head can demonstrate some signs of CVT -Dense triangle sign, empty delta sign, cord sign -!!Dx: MRI brain with MR venography!! -Or CT head with CT venography -Tx: Heparin, usually low molecular weight heparin!! (hemorrhagic transformation is not a contraindication)
40
normal pressure hydrocephalus (NPH)
-Hydrocephalus = ↑ CSF in the ventricular system and around the brain -Theory: Brain tissue itself compresses, to make room for that extra fluid , often around the white matter -White matter impairment =poor signaling between parts of the gray matter -Dementia, ataxia, urinary incontinence -“Whacky, wobbly, wet” -CT scan: Enlarged ventricles (abnormal absorption of CSF by arachnoid villa) -MRI -LP is definitive: Normal pressure!! -What other types of hydrocephalus are there? -Non-obstructive: enlarge of ventricles is due to cerebral atrophy -Obstructive hydrocephalus: tumors or shunt blockage. Do NOT LP these patients as they are at risk for herniation. -Management: Often shunt placement
41
VP shunt headache
-The most common shunt used in hydrocephalus is a ventriculoperitoneal shunt!! -IT consists of a 1-way valve, reservoir, and distal cathter that runs down the neck and chest wall into the peritoneal cavity -The valve and reservoir are palpable under the posterior scalp -VP shunt headaches -Shunt malfunction and/or infection -Kinking, obstruction, disconnection -Infection highest risk shortly after surgery -Vomiting, lethargy, severe headache, photophobia, meningism, AMS, slight change in behavior -VP shunt series x-rays to look for kinking -VP shunt tap to look for infection/obstruction
42
Which of the following is a known risk factor for subarachnoid hemorrhage?
History of T2DM History of HLD Family history of alcoholism/substance abuse in parent Sibling with history of ruptured cerebral aneurysm African American ethnicity
43
non-traumatic SAH
-Cause: Aneurysm (80%), AVM, Neoplasm -Aneurysms tend to be located on the Circle of Willis -If on posterior communicating artery leads to CN3 palsy (dilated, down, out pupil) -!Sentinel “warning” bleed! that precedes the rupture: severe HA, thunderclap, nausea, vomiting -Rupture causes acute “thunderclap” headache, vomiting, seizure, ↓ LOC, neck pain, low grade fever, possible AMS, HTN -!Pain may completely resolve with pain meds -!Pain may completely resolve by the time they get seen -!Dx: CT head (~100% sensitive within 6 hours) -LP if high suspicion and negative CT scan -More evidence now for CTA or MRA instead of LP -LP vs. CTA/MRA requires discussion -Management: -ABC stabilization -Blood pressure control to prevent bleeding from aneurysm -> SBP <160mmHg with labetalol, nicardipine, clevidipine -Reversal of coagulopathy -Thrombocytopenic (<100k platelets) -> platelet transfusion -Warfarin -> PCC and Vit K, or, FFP if prior unavailable -Prevent cerebral vasospasm with Nimodipine 60mg q4h
44
A CT head is done to evaluate a patient with a high suspicion of SAH. It’s negative. What's the next best step?
Nothing – sensitivity is high enough on CT to rule out condition Order a CT angiogram Order an MRI/MRA Perform a lumbar puncture
45
expected LP in SAH
-↑ opening pressure, ↑ RBC count, xanthochromia -Blood -In SAH, RBC count should NOT diminish from tubes 14 -A declining RBC count with successive tubes is suggestive of a traumatic lumbar tap -Xanthochromia -Pink or yellow tint -Indicates blood in the CSF at least for 2 hours -100% of SAH patients will have xanthochromia by hour 12
46
which is true regarding post lumbar puncture headaches
Pain is typically improved by sitting up and worsening with laying flat (better when flat!) Using a lower gauge needle during LP can decrease incidence Bed rest following the procedure can decrease the incidence Symptoms typically begin within 48 hours!!!!
47
peripartum HA
-MC headache peri-partum: Migraine -Life threatening differentials: -Pre-eclampsia / Eclampsia / HELLP syndrome -Check for elevated BP and proteinuria, 20 wks gestation up to 6 weeks after delivery -PRES = Posterior reversible encephalopathy syndrome -Headaches, seizures, AMS, vision loss -Diagnosed on MRI -Despite the name, not always reversible, mortality rate 15% -Cerebral venous thrombosis -Pituitary apoplexy -Thunderclap headache similar to SAH. -May have loss of visual fields or diplopia, nausea, neck stiffness, AMS -Cervical artery dissection -Non-life threatening: -!Post – LP headache that occurs ~5 days after epidural placement -Worse when upright, better when supine
48
categories of acute back pain
-non-specific lumbosacral pain/ strain -radicular pain/sciatica -emergent patho: -infection-osteomyelitis, spinal epidural abscess -cord compression- metastatic or herniation or trauma -fracture- trauma or pathologic -vascular- leaking or ruptured AAA, retroperitoneal bleed, spinal epidural hematoma
49
LBP emergent differentials
-Vascular catastrophes* -AAA -Aortic dissection -Renal artery dissection or thrombosis -Posterior abdomen: -Pyelonephritis -Retroperitoneal hemorrhage -Pancreatitis, PUD, cholecystitis -Ectopic pregnancy -Psoas hematoma or abscess -Oncologic -Intramedullary tumor -Metastatic disease -Infection* -!Spinal epidural abscess -!Vertebral osteomyelitis -!Discitis -Cord compression* -Cauda equina syndrome -Fracture with impingement -Epidural abscess -Epidural hematoma -Epidural metastatic disease -Fracture* -Traumatic -Pathologic -TUNA FISH- trauma, unexplained wt loss, neuro sx, age >50, fever, IV drugs, steroid use, hx of cancer -Sudden back pain with spinal tenderness (especially with history of osteoporosis, cancer, steroid use) -Recent spinal interventions esp. with coagulopathy
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LBP: pertinent + and -
-Infection risk factors? -IV drug abuse, spinal procedures, recent infections (e.g. endocarditis), severe unrelenting pain that is worse with lying down, fevers -Fracture risk factors? -Trauma, cancer (no matter how remote), osteoporosis, severe unrelenting pain that is worse with lying down -Cord compression symptoms? -Saddle paresthesia, bilateral paresthesia's, erectile dysfunction, progressive bilateral leg weakness or numbness, difficulty urinating/constipation, urinary/bowel incontinence. -Other red flags: -Focal neuro deficits, midline or point tenderness, weight loss, pain > 6 weeks
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low back pain exam
-Focal neurologic signs and symptoms are specific but not sensitive! -Concerning physical exam findings -Vitals – especially fever! -Motor – weakness in legs or arms – especially bilateral -Sensory – saddle anesthesia, any bilateral symmetric involvement -Reflexes – diminished or absent reflexes! including positive Babinski sign -Sphincter dysfunction – decreased rectal tone or post-void residual >100 ml -Back - Midline tenderness to palpation or percussion! -Abdomen - CVAT, pulsatile mass, guarding/rigidity -(Crossed straight leg more specific for sciatica) -Unilateral numbness/tingling along a single dermatomal distribution (e.g. L5 radiculopathy) without other red flags does NOT warrant an MRI
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localizing findings (reflex root)
-S1,S2 = Buckle my shoes! = Ankle -L3,L4 = Kick the Door! = Patellar -C5,C6 = Pick up sticks! = Biceps -C7,C8 = Lay em straight! = Triceps -L1,L2 makes testicles move = Cremasteric -S3,S4 winks galore = Anal wink reflex
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low back pain imaging
-Most LBP does NOT require imaging -Do NOT image low back pain within the first six weeks of atraumatic back pain unless red flags are present -Supportive care for MSK pain is enough! -Consider XRAYs in extremes of age, cancer, osteoporosis, new back pain in the elderly, trauma -R/O non-MSK causes of back pain -MRI indications: -Prescence of focal or progressive neurologic deficits- Singular radiculopathies can have a non-emergent MRI done outpatient -Suspicion of cord compression -Suspicion of cancer -Suspicion of infection -Presence of fever, or, elevated ESR>20 in an IDVU patient
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cauda equina and conus medullaris
-Spinal cord terminates at the conus medullaris between L1-L2 -Below this lies the nerves that make up the cauda equina -CES (cauda equina syndrome) refers to compression of these nerves -Can include the conus medullaris or the cauda equina distal to it -Herniated disc, retropulsion of bone fragments, hematoma, epidural abscess, epidural hematoma, diskitis, tumor, vascular insufficiency, spinal stenosis -!Low back pain & Sciatica (97%) -Lower extremity weakness, paresthesia's -Severe neuropathic pain -!Saddle or perineum anesthesia (92%) -!Bladder dysfunction (92%) -!Bowel dysfunction (72%) -!Sexual dysfunction (impotence in men) -Areflexic paraplegia, atrophy – late signs -Ask about RF: -!Malignancy history!, recent trauma, anticoagulation, IVDA, spinal instrumentation -Examination: -Motor or sensory deficits in the legs -Usually bilateral -Can be unilateral or asymmetrical -Lower motor neuron signs in chronic cord compression : areflexia, hypotonia, atrophy -Saddle anesthesia -↓ or absent rectal tone -Abdomen = large bladder
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cauda equina dx and tx
-Imaging -!!STAT MRI cord-compression series = gold standard! -CT myelogram if unable to obtain MRI (metal implants) -Consider post-void residual (>100cc generally neurologic) -Management: -Neurosurgical emergency!!! -Technically a clinical diagnosis -> STAT consultation (even before MRI if high suspicion) -Steroids if metastatic cause -Decompression within 24 hrs window
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spinal epidural abscess
-Suspect in patients with: -Back pain + neuro deficits, fever, immunocompromised, recent spinal procedure -Risk factors: DM, IVDU, indwelling catheters, recent spinal intervention, infection elsewhere, immunosuppression, repeat ER visit -ESR/CRP -ex. pt with recent LP presents with back pain but no fever -> check ESR/CRP to see if its an early infection -CT CANNOT r/o abscess – may only show osteomyelitis -!!MRI of C/T/L spine -Do not delay antibiotics -Emergent drainage/decompression by neurosurgery
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spinal metastasis
-Known cancer + new low back pain -Spinal metastases until proven otherwise -MCC of spinal compression -Emergency: cord compression -Dexamethasone 10mg IV if neuro sxs present -Urgent MRI
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spinal epidural hematoma
-After spinal procedure -Spontaneous or traumatic - anticoagulation, hemophilia’s -Spinal cord compression symptoms depend on extent of hematoma
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AAA rupture
-Abdominal pain, back pain, pulsatile abdominal mass -Other symptoms: Dizziness, syncope, groin pain, flank mass, poor circulation -Red flag: Syncope after pain onset, presentation in shock (hypotension) -POCUS for AAA
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retroperitoneal bleeds
-Consider in coagulopathies, retroperitoneal masses/tumors, abdominopelvic trauma -Blood in the retroperitoneal space can cause back pain, abdominal pain, hip/groin/anterior thigh pain -Psoas sign = positive in retroperitoneal irritation -Cullen/turner sign -Bruising or swelling in groin due to extension of bleeding
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simple lumbosacral sprain / mechanical low back pain
-Dx of exclusion after thorough history and physical ± imaging -NSAIDs, acetaminophen, heat, massage, PT, consider muscle relaxers -Education: Mechanical problem = mechanical solution -Active movement -No strict bed rest -Reassurance
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A 16 year-old Hemophilia A patient is complaining of back pain and unable to move his right hip a few days after a soccer game. On exam the abdomen is unremarkable, and he holds his right hip flexed with a pillow under his thigh. Any attempt at passive or active extension of the hip causes excruciating back pain. Pain is minimal if patient avoids movement. No distal neurologic findings or saddle hypoesthesia are detectable. Lumbar X-ray is insignificant. What is the best next step for this patient?
NSAIDS and opiates Factor VIII concentrate and abdominopelvic CT Scan!!! Pelvic x-ray and hip reduction Emergent MRI of the hip -concern for retroperitoneal bleed in abdomen or hip
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seizures
-Make up 1% of all ED visits -breakthrough seziures- infection, drug use (ilicit or prescribed), noncompliance, ALCOHOL -Acute and chronic triggers: hemorrhage, cerebral injuries, tumors, infections, metabolic derangement, congenital causes of epilepsy -Not all are generalized convulsive… absence, simple partial, complex partial -!Status epilepticus!: ACEPT 2014 definition -!!!!!!!Unremitting convulsive seizure activity lasting 20 minutes or more, or, -!!!Back-to-back seizures without regaining full consciousness in between , or, -!!A generalized convulsive seizure lasting ≥ 5 minutes !!!!!!!! -MC trigger: Subtherapeutic drug!!! levels of anti-convulsant! -Intoxication, withdrawal, trauma, meningitis, psychiatric issues, metabolic derangement etc.
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seizure workup
-Pts with seizures who are back to baseline (e.g. they are not currently seizing): -POC Glucose -Electrolyte and CBC check -Pregnancy test -First time seizure- CT / MRI -History of epilepsy: -Anti-epileptic drug levels -Assessment for other triggering factors (lack of sleep, change in meds, vomiting) -Consider a loading dose of anti-epileptic in patients who are subtherapeutic
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management of active seizures
-!!*Check the glucose -!!!1st line = Benzodiazepines: IV Lorazepam (ATIVAN) -Adult dose: 4mg IV push over 2 minutes -Pediatric dose: 0.1mg/kg IV push -!!Repeat in 5-10 minutes if needed -Alternatives: Diazepam 10mg IV/PR, midazolam 10mg IV/IM/IN -2nd line = Phenytoin load!! 20mg/kg IV over 20 minutes Takes 20-30 minutes to work, start as soon as status epilepticus is suspected -3rd line = !!!Propofol 1.5mg/kg IV -Rapid sequence intubation is recommended if patient is non-responsive to first few doses of benzos, as they are likely going into status epilepticus -Search for reversible causes
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a pt with PMH for tuberculosis on INH presents with a first time seizure. is there any connection
-INH = injuries neurons and hepatocytes -consider giving vit B6 (pyridoxine) to stop convulsions