Head Impulse Test in Stroke vs. Vestibular NeuritisNewman-Toker/Kattah

Normal Head Impulse Test Differentiates Acute Cerebellar Strokes from Vestibular Neuritis

Newman-Toker*, Kattah,*Alvernia, Wang (Neurology, 2008) * denotes co-first authorship

Online Appendix 4 – Video Legends

This Appendix contains a brief introduction to conducting the head impulse test and the video legends for the three videos that accompany the above-mentioned manuscript.

Brief Introduction to Conducting the Head Impulse Test

The horizontal head impulse test (h-HIT) of vestibulo-ocular reflex (VOR) function, as originally described, is a rapid, passive head rotation from a center to lateral (10-20 degrees) position as a subject fixates at a central target (e.g., the examiner’s nose). A common adaptation of the h-HIT, used in this study, is to displace the head laterally first, then rotate the head back to the center position. Some examiners find the maneuver easier to conduct using this centripetal head motion, and the results are sometimes easier to interpret (since the globes end in the primary position in the orbit, rather than a somewhat lateral position). This approach also reducesany theoretical risk of vertebral artery injury withneck over-rotation by an overzealous, inexperienced examiner.

Although not originally validated with a lateral to center rotation, there is no compelling reason to believe that the vestibular system should respond differently, since the VOR response should be largely independent of the starting position of the head on the neck. During videotaping, the amplitude of the h-HIT head rotation was exaggerated in an attempt to enhance its visibility. It is recommended that the test be performed clinically using a smaller-amplitude movement.

The normal VOR response to a rapid, passive head rotation as a subject fixates at a central target (e.g., the examiner’s nose) is an equal and opposite eye movement that keeps the eyes stationary in space (i.e., still looking straight at the target) (negativeh-HIT). An abnormal response occurs when the head is rapidly rotated toward the side of a vestibular lesion. The loss of vestibular input results in the subject’s inability to maintain fixation during the head rotation, requiring a corrective gaze shift once the head stops moving (positiveh-HIT). For the practitioner, it is crucial to remember that for the test to work, the head rotation must be passive (i.e., conducted by the examiner), rather than active (i.e., deliberate head turn executed by the patient).

VIDEO LEGENDS

Video 1

Typical APV with left-beating, unidirectional nystagmus and abnormal rightward h-HIT

Corresponding Case: Appendix 3, Table A3-1, Case 8

Video Timing: video taken 26 hours after symptom onset, within 1 hour of initial examination

Case Description: A 54-year-old man with a history of diabetes mellitus on diet-control presented with a 24-hour history of vertigo, falling to the right, nausea and vomiting, without auditory symptoms.He displayed a primary gaze, unidirectional, left-beating nystagmus that increased when looking in the direction of the nystagmus fast phase (i.e., in left gaze), and with fixation removal, both findings typical for a (right) peripheral vestibular lesion.He had an abnormal (positive) h-HIT to the right, and a normal (negative) h-HIT to the left, as anticipated. In the video, the rightward h-HIT is demonstrated first, with a pathologic, leftward, re-fixation saccade evident at the end of the head rotation, indicating a failure of the normal vestibulo-ocular reflex response to keep the eyes steady on the target (i.e., the video camera lens). The leftward h-HIT is demonstrated next, with no refixation saccade evident at the end of the head rotation, indicating an intact vestibulo-ocular reflex response.The head MRI showed an incidental, 4 millimeter area of increased signal in the periventricular white matter, but no acute infarct by DWI.The diagnosis was right APV.Note that the subtle flattening of the left nasolabial fold apparent on the video was old (lifelong) and unrelated to his acute vestibular syndrome.

Video 2

APV mimic, with pseudo-labyrinthine nystagmus, but normal h-HIT, suggesting stroke

Corresponding Case: Appendix 3, Table A3-2, Case 1

Video Timing: video taken 18 hours after symptom onset, 12 hoursafter initial examination

Case Description: A 71-year-old hypertensive man presented with a two-hour history of ataxia, nausea and vomiting without auditory symptoms.He fell to the left when standing.He had right-beating nystagmus in right gaze, but no nystagmus in primary or left gaze.Fixation removal showed a unidirectional, primary gaze, right-beating nystagmus that increased in right gaze, compatible with a peripheral-type nystagmus.However, the h-HIT was normal (negative), decreasing the likelihood of APV substantially, and suggesting a pseudo-labyrinthine presentation of stroke. The video, obtained 12 hours later, demonstrates saccadic rightward horizontal pursuits, but relatively smooth leftward pursuits. Fixation removal revealed a subtle oblique/down-beating component to the nystagmus, but the dominant vector remained horizontal and right-beating.Head CT scan showed a right inferior cerebellar stroke, associated with moderate mass effect and fourth ventricular compression (manuscript Figure 2, panel A).Three days later, on repeat assessment (not shown), there was gaze-evoked nystagmus to the right and very subtle right-shoulder-beating torsional nystagmus in left gaze, but nil in primary, up, and downgaze. With fixation suppression he had a more obvious oblique (right-down) beating nystagmus in primary gaze and down-beat positional nystagmus. The h-HIT remained normal.An open MRI obtained one month later (Figure 2, panel B) showed an area of encephalomalacia involving the right inferior cerebellum, confirming the prior infarct evident by CT acutely.

Video 3

APV mimic, with pseudo-labyrinthine nystagmus and abnormal h-HIT, but evolution of additional oculomotor and neurologic signs, confirming stroke

Corresponding Case: Appendix 3, Table A3-5, Case 1

Video Timing: video taken approximately 1 year after symptom onset and initial examination

Case Description: A 56-year-old hypertensive, diabetic woman presented with a 6-hour history of acute vertigo without auditory symptoms.She fell to the right while standing, and had nausea and vomiting.On initial examination (not videotaped), she had a unidirectional, left-beating nystagmus that increased with gaze left and fixation removal, and an abnormal (positive) h-HIT to the right, all consistent with a bedside diagnosis of right APV.In the ensuing hours, she developed a right infranuclear facial paresis, saccade hypermetria, and bidirectional nystagmus, suggesting a central lesion and false initial lesion localization. A brain MRI demonstrated a stroke involving the right lateral pons and right middle cerebellar peduncle (manuscript Figure3, panel A).Follow-up general neurologic examination revealed increasing truncal and right upper extremity limb ataxia. Follow-up CT scan was obtained 2 days later (Figure3, panel B), revealing an extensive stroke involving much of the right cerebellar hemisphere, with mass effect.At one-year follow-up, she still could not stand, remained dysarthric, and had persistent, direction-changing, gaze-evoked nystagmus. Her primary gaze nystagmus at one-year follow-up, evident only with suppression of visual fixation, had become right-beating behind Frenzel goggles (not shown). The h-HIT remained abnormal (positive) to the right, continuing to represent a false localizing sign to the periphery.Repeat MRI, one year after the initial stroke, showed a large area of encephalomalacia in the region of the right cerebellar hemisphere.The abnormal oculomotor and vestibular findings persisted for 5 years until the patient’s death.

Online Appendix 4 – Video LegendsPage 1 of 3