HiNTS exam


Series of three quick, bedside, physical exam maneuvers that can potentially rule out a central cause of vertigo


Hi for head impulse testing, or head thrust testing.
N for nystagmus to remind you to look for direction-changing or vertical nystagmus
TS for test of skew.





  • Nearly two-thirds of patients with stroke lack focal neurologic signs that would be readily apparent to a nonneurologist

  • Presence of all three “reassuring” exam findings suggests it can be ruled out with a 100% sensitivity for ischemic stroke in AVS while an initial MRI with diffusion-weighted imaging (DWI) had a 88% sensitivity



Maneuvers used to help distinguish between central and peripheral vertigo in patients experiencing an acute vestibular syndrome (AVS) which is best defined as: rapid-onset vertigo, nausea and/or vomiting, gait unsteadiness, head motion intolerance, and nystagmus.



The patient must be experiencing continuous vertigo for the results to be reliably interpreted.


Head Impulse Test


  • Ask the patient to relax his/her head and maintain his/her gaze on your nose. Gently move the patient’s head to one side, then rapidly move it back to the neutral position. The patient may have a small corrective saccade. The head impulse test is positive (consistent with peripheral vertigo) if there is a significant lag with corrective saccades. If you can see the correction, it is abnormal. Compare this to the contralateral side; a difference in the speed of correction should be noted.

  • In acute vestibular syndrome, an abnormal result of a head impulse test usually indicates a peripheral vestibular lesion, whereas a normal response virtually confirms a stroke.

  • Abnormal exam rules in peripheral vertigo and thus rules out central vertigo if only unilateral

  • Video- https://www.youtube.com/watch?v=XpghlvnrREI&feature=youtu.be&t=665



  • Note if it is present in primary gaze (i.e. looking straight ahead) and or in lateral gaze. Unidirectional, horizontal nystagmus is reassuring for peripheral vertigo where as purely bidirectional, vertical or torsional can be consistent with central cause

  • The most common peripheral nystagmus, BPPV, in the posterior semicircular canal consists of a unidirectional horizontal nystagmus with a torsional component.


Test of Skew

  • Have the patient maintain his/her gaze on your nose. Alternate covering each of the patient’s eyes

  • Positive result will be the deviation of one eye while it is being covered, followed by correction after uncovering it.




  • If the HiNTs exam is entirely consistent with peripheral vertigo (positive head impulse test, unidirectional and horizontal nystagmus, negative test of skew), then, according to the derivation paper, it is 100% sensitive and 96% specific for a peripheral cause of vertigo.

  • Use of HiNTs exam in the ED is currently controversial as the primary study was performed by neurologists in a partially differentiated patient population

  • likely has higher utility in the patient population in whom the clinician suspects a peripheral cause of their vertigo to rule out central cause and limit needless imaging




  • Do not perform on any patient that has head trauma, neck trauma, an unstable spine, or neck pain concerning for arterial dissection.

  • Do not perform in patients with known severe carotid stenosis as it may embolize unstable plaque

  • Challenging to differentiate between catch up saccade and nystagmus

  • Patients with acute active AVS likely to not tolerate the testing

  • Patient must be awake and cooperative.

  • Essentially an awake “doll’s eye” that requires conscious fixation on an object. Cannot perform on mentally impaired or sedated patients

  • Not yet been validated by a large external group, let alone a large external group of emergency medicine providers.

  • In the study, exam performed by ophtho neurologists






Nelson, James A., and Erik Viirre. "The clinical differentiation of cerebellar infarction from common vertigo syndromes." Western Journal of Emergency Medicine 10.4 (2009): 273.

Kattah, Jorge C., et al. "HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging." Stroke 40.11 (2009): 3504-3510.

Tarnutzer, Alexander A., et al. "Does my dizzy patient have a stroke? A systematic review of bedside diagnosis in acute vestibular syndrome." CmAJ 183.9 (2011): E571-E592.


POTD: Idiopathic Intracranial Hypertension

POTD: Idiopathic intracranial hypertension


Idiopathic intracranial hypertension (IIH) aka pseudotumor cerebri and benign intracranial hypertension

·      rare condition

·      presents with gradual onset and chronic headache, vision changes, nausea, vomiting, and tinnitus

·      + papilledema/ swelling of the optic disc on fundoscopy

potd eye papill.jpg

·      optic sonography

potd us eye.jpg
  • ONSDs should be measured 3 mm behind the papilla, an average of less than 5 mm is considered normal.

  • ONSD > 5 mm has been shown to be 90% sensitive and 85% specific for ICP > 20.

·      Classic presentation: young, obese female

·      + association has been found with this diagnosis and the use of oral contraceptive medications, tetracycline, anabolic steroids, and vitamin A

·      Pathophysiology is not well understood but thought to be caused by an imbalance in CSF production and reabsorption

·      Diagnostic criteria include an alert patient with either a normal neurologic examination or findings consistent with papilledema, visual field defect, or an enlarged blind spot

·      Definitive dx: Lumbar puncture

  • done in a recumbent position reveals an elevated CSF opening pressure of more than 20 mm Hg in an obese patient (normal being up less than 20 mm Hg).

  • normal CSF analysis.

·      CT head may show “slit like” or normal ventricles without mass effect

·      DDx: glaucoma, venous sinus thrombosis, ICH, IC mass.

·      Treatment

  • Repeat LPs  

  • Acetazolamide

  • Surgical shunt if severe and refractory

  • offending agents such as oral contraceptive medications should be discontinued.

·      Permanent loss of vision can occur in up to 10% of patients, and higher if left untreated




  • Dubourg J, Javouhey E, Geeraerts T, Messerer M, Kassai B. Ultrasonography of optic nerve sheath diameter for detection of raised intracranial pressure: a systematic review and meta-analysis. Intensive Care Med. 2011;37(7):1059-68. [pubmed]

  • Blaivas M, Theodoro D, Sierzenski PR. Elevated intracranial pressure detected by bedside emergency ultrasonography of the optic nerve sheath. Acad Emerg Med. 2003;10(4):376-81. [PDF]

  • https://www.ultrasoundoftheweek.com/uotw-5-answer/

  • Peer IX


POTD: Straight leg test. A leg up on clinical testing!

A little background:

Lumbar disc herniation is the most common cause of lumbar radiculopathy, or sciatica, a shooting or burning pain from the low back radiating down the posterior leg distal to the knee.

Two tests used to evaluate these symptoms are

The straight leg raise.

·       The straight leg raise test is highly sensitive but not very specific for disc herniation.

·       This is performed by lifting the leg affected by the radiating pain.

·       The patient lies supine with one leg either straight or flexed at the knee with the sole of the foot flat on the stretcher.

·       The examiner then raises the affected leg up, extended, to 30 to 70 degrees.

·       Reproduction of low back pain that radiates down the posterior affected leg at least past the knee is considered a positive result. Not just pain to the lower back, which is a common misconception.

·       The SLR test can also be performed with the patient in a sitting position, by stretching the sciatic nerve by extending the knee; the test is positive if pain radiates to below the knee.


The crossed straight leg raise.

·       It is highly specific (90%) for disc herniation

·       You perform the same test as the straight leg but on the unaffected leg.

·       A positive test: reproducing both the back pain + the radiation down the affected leg.

Sources: Peer IX, Tintinelli’s, Dr. Sergey Motov, Uptodate


POTD: Cervical Artery Dissection

Clinical Scenario:

A 25-year-old woman presents with neck pain, headache, nausea, left-sided facial numbness, and an unsteady gait. She says the headache began 7 days earlier shortly after a chiropractic treatment for chronic neck pain. Vital signs are normal; the unsteady gait is noted on ambulation. Noncontrast head CT findings are normal.

Which of these tests should be ordered next?

A. CT angiography of the neck with contrast

B. CT of the neck without contrast

C. Duplex ultrasonography of the carotid arteries

D. Duplex ultrasonography of the vertebral arteries.

The answer is A

Cervical Artery Dissection

What is it?

  • Cervical artery dissections is the collective term for dissections of the carotid or vertebral arteries

    • internal carotid artery is most commonly affected

    • vertebral artery dissections are uncommon

  • Dissection of the cervical arteries is a common cause of stroke among young and middle-aged persons

    • ~ 20% of strokes in the young are caused by carotid artery or vertebral artery dissections in the neck, compared to only 2.5% in older patients

  • Caused by minor trauma in the setting of neck manipulation (e.g. by a chiropractor) or a minor sports injury. There are some case reports of these injuries occurring from riding roller coasters. 

  • Seen more commonly in patients with connective tissue disorders or vascular pathologies (e.g. HTN, Marfan’s syndrome, fibrocystic dysplasia, etc)



  • Classic presentations include neck pain and headache that might precede development of neurologic symptoms (hemiplegia, hemisensory loss) by hours or up to 14 days.

  • Vascular bruits (absence does not exclude dissection, e.g. present in only about 1/3 of carotid dissections)

  • carotid dissection tends to present with some or all of the following:

    • frontal headache

    • anterior neck pain

    • eye, ear, or face pain

    • Ipsilateral Horner’s syndrome (due to expansion of the internal carotid artery with compression of sympathetic nerve fibers)

  • vertebral artery dissectiontends to present with some or all of the following:

    • occipital headache

    • posterior neck pain

    • unilateral facial numbness, dizziness, ataxia, vision disturbances (diplopia), and nausea or vomiting


  • Diagnosis is via CT angiography of the neck. Although it might take longer to obtain, MRA is also an acceptable diagnostic test. 


  • Anticoagulation with heparin intravenously followed by warfarin.

  • tPA may be considered in some patients with stroke due to spontaneous extracranial dissection

  • Endovascular therapies include stenting

    • usually used for extracranial carotid or vertebral artery dissection when medical management fails or is contraindicated

    • improved outcomes are associated with reconstitution of flow within 6 hours




POTD: Trauma Tuesdays - Concussions

Clinical scenario:

A 16-year-old boy presents after hitting his head in a collision with another player during a soccer game. He denies loss of consciousness but complains of a moderate headache, nausea, and difficulty concentrating. 

Which of the following represents appropriate next steps in management?

A. Admit the patient to the hospital for overnight observation

B. Clear the patient to play after 48 hours if his symptoms resolve

C. Discharge with instructions to get follow-up care and not return to play

D. Order a head CT to rule out the presence of an intracranial bleed or swelling

The correct answer is C. 


What is a concussion?

The term "concussion" is often used in the medical literature as a synonym for mild TBI but more specifically describes a pathophysiological state that results in the characteristic symptoms and signs that individuals may experience after a mild TBI. 


Rapid-onset short-lived neurologic function impairment that resolves on its own. These symptoms reflect functional disturbance rather than structural injury.

concussion symptoms.png


If one or more of the following:

  • Symptoms, including somatic (headache, nausea, off balance), cognitive (“ in a fog,” slow), or emotional (rapidly changing)

  • Physical signs, such as loss of consciousness, amnesia, although LOC is not required

  • Behavior changes, such as irritability

  • Cognitive impairment, such as slowed reaction times

  • Sleep disturbance, such as insomnia


  • Concussion is a clinical diagnosis, and there are a variety of sideline assessment tools (that are outside the scope of the ED) that include measurements of orientation, symptoms, gross cognition, and physical examination findings (e.g. Standardized Assessment of Concussion (SAC)Balance Error Scoring System (BESS), computerized neurocognitive testing, and the Sport Concussion Assessment Tool version 5 (SCAT5 or Child-SCAT5)).

  • Physical exam should include: 

    • assessment of the cervical spine (+/- immobilization with c-collar if cervical spine injury suspected)

    • detailed neurologic assessment (including mental status, cognitive functioning, and gait/balance)

    • structural brain imaging (i.e. CT scan or MRI) if concern for structural injury (e.g. acute brain bleed)

Discharge Precautions

This is arguably the most important part of your role in the concussed patient. Thankfully, the CDC has a ton of great literature on the subject.

Pediatric Care Packets:

  1. Pediatric Discharge Instructions

  2. Symptom-Based Recovery Tips

  3. Pediatric Care Plan

Adult Care Packets:

  1. Adult Concussion Fact Sheet

  2. Adult Concussion Brochure

  3. Adult Care Plan







POTD: Cerebral Venous Sinus Thrombosis (CVST)

Clinical Presentation:

An 18-year-old female student presented with a 7-day history of worsening frontal headache and 1 day history of vomiting. The patient described marked photophobia, but no fever or history of seizure. She was taking a combined oral contraceptive and had no other medical history. Physical examination showed no focal neurology, but fundoscopy revealed bilateral papilledema. 

Today, let’s learn about cerebral venous sinus thrombosis.

What is it?

Clot that forms within the major cerebral veins, such as the dural sinuses (super sagittal sinus, straight sinus, and transverse sinuses), cortical veins, vein of Galen, and jugular veins.


What causes it?

Thrombosis of either the cerebral veins or of the major cerebral sinuses.


  • More common in younger patients (median age = 38)

  • More common in women

  • Mortality of 10-30%

  • Risk factors: 

    • Acquired: infections (otitis, mastoiditis)surgerypregnancy, trauma, cancer, exogenous hormones

    • Genetic: inherited thrombophilia


  • Non-specific stroke-like symptoms: severe HA (90% of patients) that can be gradual in onset, weakness, paresthesias, blurred or double vision

  • If increased ICP, can see mental status changes, lethargy, decreased consciousness, papilledema 

  • If focal brain injury, can have seizures or focal neurological defecits


  • Variety of imaging modalities for diagnosis, typically can start with a non-contrast CT head and then progress to CT venogram (if MRI unavailable), or perform MR venography, MRI, or cerebral angiography


  • Manage seizures or herniations 

  • Start anticoagulation

    • Unfractionated heparin (UFH)

    • Low molecular weight heparin (LMWH): 1 mg/kg SQ Q12 hours

  • Other treatment modalities: systemic thrombolytics, cather-based interventions (thrombolytics and thrombectomy), decompressive craniectomy


Targeted Temperature Management

Targeted Temperature Management

What is it: the purposeful cooling of a patient post-cardiac arrest. Target of 32°C to 34°C (Some studies say 36, but debatable and prevent any hyperthermia) for at least 24 hours. 

Why: To improve the chance of survival and neurologic recovery, international guidelines recommend use of targeted temperature management (TTM), together with urgent coronary angiography and percutaneous coronary intervention when appropriate


  • Post cardiac arrest (any cause but most evidence supports from VF/VT shockable causes of cardiac arrest)

  • ROSC < 30 mins from team arrival

  • Time < 6 hours from ROSC

  • Patient is comatose, GCS <8 (this is try and improve neurological outcome, so someone who is neurologically intact does NOT need TTM)

  • MAP >= 65mmHg

  • depends on your hospital protocol

When: Initiate within 6 hours of ROSC and maintain for 24 hours


  • cold IVF at 2-3 mL/kg stat

  • cooling vest and cooling machine

  • sedation and paralysis



Shivering, electrolyte abnormalities, cold diuresis, infection. 


So, for post cardiac arrest patients with depressed neurological function - Keep this in mind, but consult your ICUs and plan this patient's care together for best management. TTM needs an ICU level care admission. 

Happy Learning!






Mobile Stroke Unit

My dear BK docs: 

The Mobile Stroke Treatment Unit (MSTU) is operational in Brooklyn now.

So it is highly likely that eventually you will receive a patient who has received thrombolysis in the field for a presumed ischemic stroke. They are operational 9a-5pm and are dispatched by FDNY.

They have been active since June, and respond to 2-3 calls a day along a BLS unit. They are dispatched to the scene if the story is concerning for a critical CVA (CVA-C).

They will push t-Pa and start the infusion if after neurologist assessment they meet t-Pa criteria.

The Brooklyn NYU MSTU crew report pushing t-Pa in the field 15 times since beginning operation.

The crew consist of 2 paramedics, a ct technologist, a nurse, and a neurologists who performs a remote assessment using multiple cameras in the back of the unit.

Please understand that the data supporting use of this technology for the benefit of a patient in an urban setting is controversial and not well studied. The data supporting this approach to stroke management in a rural setting is also controversial. But the primary theory is that it will increase the probability that a patient with a significant stroke will initially be transported to a hospital capable of mechanical thrombectomy or other endovascular approaches. Anything deeper is beyond the scope of this pearl of the day.

Now for a quick review of t-Pa, based on a synthesis of NINDS and ECASS:

Indications for t-Pa:

-acute ischemic stroke with onset less than 4.5 hr

-must have NIH stroke scale <25, but with significant deficit, eg aphasia, RUE paralysis, etc. A caveat here is that a patient with a basilar artery occlusion may have a very high stroke score, but they should get t-Pa (and likely mechanical thrombectomy; again too deep of a topic for a pearl of the day).

-No ICH on head CT

Contraindications to t-Pa:

-stroke or ICH in past 3 months

-Severe stroke NIHSS>25; the thought here is a stroke that is greater than 1/3 MCA territory will have high post-ischemic bleeding potential

-surgery within past 14 days (this has to be “major”)

-Systolic BP > 185 (you can control this prior to t-Pa administration)

-history of ICH

-rapidly improving symptoms

-Combination of previous ischemic stroke WITH diabetes

-minimal symptoms (eg paresthesias in the hand)

-GI/GU bleed in past 21 days

-platelet less than 100k

-arterial puncture at non-compressible site last 7 days (eg, subclavian a-line, extremely rare)

-seizure with onset of stroke

-on anticoagulation

Relative contraindications

-age greater than 80 (I moved this from ECASS III absolute contraindications, mostly because of our patient population)

-recent LP

-Recent MI

-glucose less than 40 or greater than 400 because this suggests metabolic; caveat here, if hypoglycemia is corrected need to more strongly consider stroke.

-post MI pericarditis

-Recent MI less than 3 months ago

-if a patient has a history of veno-hepato/renal occlusive disease or TTP and is defibrotide for treatment of any condition, you should consider witholding t-Pa. This drug is though to enhance plasmin activity, thereby helping to prevent clot propagation and promote reabsorption. FYI: you may never see a patient on this drug.


-t-Pa is dosed at 0.9 mg/kg (max 90), give a 10% bolus with the remainder to be infused over 1 hr.


If and when a thrombolysed patient comes from the field into the ED, you need to be prepared from the complications of administration of these agents.

The mechanism of action of alteplase is to “enhance the conversion of plasminogen to plasmin by binding to fibrin, initiating fibrinolysis with limited systemic proteolysis”. This essentially is the “clot-buster"

Hypersensitivity reaction is also possible. So be prepared to give epi IM if signs of anaphylaxis develop.

However, the most significant and common side effect you must monitor for is HEMORRHAGE, give FFP or cryoprecipitate. Give crossmatched blood if bleeding has stabilized and is indicated. Start MTP if is massive. Rate of GI bleed is as high as 5%.

Other clinically significant hemorrhages include ICH (0.4-1.3%). This may result in herniation (very rare).

Another rare complication is cardiac tamponade. If a patient has an ischemic stroke and has a history of cardiac ablation AND is no longer anticoagulated, you should suspect pericardial effusion/tamponade if there are ANY changes in their hemodynamic status.

FINAL CAVEAT: ask the stroke EMS crew for labs if they drew them. They should be drawing them because coagulation studies may become deranged after t-Pa administration.