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Complete Heart Block Complicating the Head Impulse Test FREE

Edward Ullman, MD; Jonathan A. Edlow, MD
[+] Author Affiliations

Author Affiliations: Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts.


Arch Neurol. 2010;67(10):1272-1274. doi:10.1001/archneurol.2010.266.
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Published online

Background  Symptoms of acute vestibular syndrome include dizziness, nausea, vomiting, and postural instability. The cause may be a peripheral or central lesion. Distinguishing between these two causes is critical because the treatments differ completely. One bedside test to help make this distinction clinically is the head impulse test (HIT), sometimes called the head thrust test.

Objective  To describe a case of complete heart block associated with performance of the HIT.

Design  Case report.

Setting  Academic medical center.

Patient  A 52-year-old woman presented to the emergency department with sudden onset of dizziness.

Intervention  The HIT.

Main Outcome Measure  Use of the HIT to help distinguish between a peripheral or central lesion in a patient with dizziness.

Results  Complete heart block occurred immediately after performance of the HIT.

Conclusions  Physicians may perform this test in an office, emergency department, or inpatient setting and should be aware that occasionally patients may have a severe vagal reaction including complete heart block.

Figures in this Article

Symptoms of acute vestibular syndrome (AVS) include dizziness, nausea, vomiting, and postural instability. The cause may be a peripheral or central lesion. Distinguishing between these two causes is critical because the treatments differ completely. Patients with vestibular neuritis benefit from steroids, while those with cerebellar stroke need treatment of the underlying vascular lesion and close monitoring for posterior fossa swelling and brain stem compression.1,2 Pilot data suggest that misdiagnosis of cerebellar infarction may be associated with worse outcomes.3

One bedside test to help make this distinction clinically is the head impulse test (HIT), sometimes called the head thrust test. This test of the vestibular-ocular reflex was first described in 1988.4 The examiner stands in front of the patient, who is seated directly in front of and facing the examiner. The patient is instructed to fixate his or her gaze on the examiner's nose and to allow the examiner to move the patient's head freely (ie, the patient must be completely passive). The examiner then rapidly rotates the patient's head 15° to 20° while carefully watching the patient's eyes. This is repeated several times in each direction.

The normal response (intact vestibular-ocular reflex, compatible with stroke) is for the patient's eyes to remain focused on the examiner's nose. The abnormal response, due to loss of vestibular input (deficient vestibular-ocular reflex, compatible with vestibular neuritis), is for the eyes to move with the head and then snap back to the target in 1 corrective saccade.

To our knowledge, there have been no reported complications reported from using this simple-to-perform bedside maneuver. We describe a patient who developed complete heart block immediately after the HIT was performed.

A 52-year-old woman presented by ambulance to the emergency department with severe dizziness. She woke up to go to the bathroom and felt the sudden onset of a loud pounding in her left ear followed by dizziness. She reported multiple episodes of vomiting especially provoked by any movement. She denied any numbness, weakness, chest pain, or shortness of breath. Her medical history was significant for similar episodes of vertigo, pituitary microadenoma, and vasovagal syncope. She was a social drinker and a nonsmoker. Approximately 10 days prior, she had been treated with azithromycin for an upper respiratory tract infection.

Her temperature was 36.7°C, her pulse was 71 beats/min, her blood pressure was 118/63 mm Hg, her respiratory rate was 12 breaths/min, and her oxygen saturation was 98% on room air. She preferred to lie on her left side with her eyes closed. Cardiac and pulmonary examination results were unremarkable. Cranial nerves II to XII were intact, and her strength was 5/5 in the bilateral upper and lower extremities. Sensory examination results were unremarkable. Deep tendon reflexes were 2+ bilaterally throughout. Formal cerebellar testing results were normal, but the patient could not walk owing to her severe dizziness. She had unilateral horizontal nystagmus.

Results of a noncontrast head computed tomographic scan were negative. The patient was given lorazepam, 2 mg, with partial relief of symptoms. To help distinguish a central process from a peripheral process, we performed the HIT. When the patient's head was rapidly rotated to her right, her eyes lost fixation on the examiner's nose; within 1 to 2 seconds, her eyes snapped back to the examiner's nose in a single corrective saccade. Within 5 to 10 seconds, the patient became diaphoretic and lost consciousness. The cardiac monitor (which initially showed sinus rhythm) now showed complete heart block, which resolved within another 30 seconds without any intervention (Figure).

Place holder to copy figure label and caption
Figure.

Cardiac monitor showing sinus rhythm on arrival (A) and complete heart block immediately after the head impulse test (B).

Graphic Jump Location

An electrophysiological study showed no evidence of atrioventricular nodal conduction abnormalities or hypersensitive carotid sinus reflex, and the cardiologist concluded that the transient high-degree atrioventricular block was secondary to vagal response. The patient improved with fluids and meclizine hydrochloride and was discharged from the hospital with the diagnosis of peripheral vertigo and a vasovagal event.

We report the first complication of the HIT to our knowledge. This test is an important part of the bedside evaluation of patients with AVS. A positive test result (loss of fixation on the target followed by a corrective saccade of the eyes) indicates a loss of vestibular function on the side toward which the head is rotated and is highly predictive of a peripheral cause such as vestibular neuritis. A negative test result (normal fixation on the target and absence of a corrective saccade) suggests that a posterior circulation stroke is causing AVS. Physicians may perform this test in an office, emergency department, or inpatient setting and should be aware that occasionally patients may have a severe vagal reaction including complete heart block.

One possible explanation for our patient's symptoms is a hypersensitive carotid sinus reflex; however, this was specifically tested for and not found at the electrophysiology study. Another theoretical concern that has been raised about the HIT is the possibility of causing an acute cervical artery dissection.5 Given our patient's lack of neck or head pain, lack of neurological findings, and clinical course, it is also unlikely that arterial dissection caused her symptoms. We believe that the complete heart block was the result of vagal stimulation from her dizziness, abruptly increased by performing the HIT.

Recent studies have shown the HIT to be very useful in distinguishing vestibular neuritis (in which the HIT result is positive) from cerebellar and other brain stem strokes (in which the HIT result is typically negative).57 While a positive HIT result strongly suggests a peripheral cause, it should not be used in isolation. This is because occasionally patients with central vestibular lesions will have a positive HIT result secondary to lesions affecting the vestibular nerve root entry zone in the pons or at the level of its nucleus. In one small study,5 9% of patients with a central cause of their AVS had a positive HIT result.

In these instances, however, other tests such as quality of the nystagmus, presence of skew deviation, other central findings on examination, and degree of ataxia will help to make this distinction between a peripheral cause of AVS and a central one.7 Specifically, patients with peripheral vestibular disease have horizontal direction–fixed nystagmus, whereas patients with vertigo from a central cause will often have nystagmus that is either vertical or horizontal direction changing. Skew deviation is rarely seen in peripheral vestibular disorders. Other central findings such as speech, motor, sensory, and visual deficits suggest a central cause.8 Severe ataxia in which the patient cannot walk or sit unassisted or unsupported also suggests a central cause.7,9 Therefore, in the presence of these other suspicious findings, even patients with a positive HIT result should be investigated for a central cause of AVS.

Accumulating evidence suggests that the HIT is a very useful clinical test, and we believe that it should be used in the evaluation of patients with AVS.57 The results of the HIT should be interpreted in the context of other findings such as other neurological examination findings, presence of vertical skew deviation, quality of nystagmus, and degree of gait instability.1,79 When performing the HIT, however, we do caution physicians to be aware of this complication especially in patients with slow underlying heart rates, receiving calcium- or β-blockers or other atrioventricular nodal blocking medications, or with known history of severe vagal sensitivity.

Correspondence: Edward Ullman, MD, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, One Deaconess Road, Boston, MA 02115 (eullman@bidmc.harvard.edu).

Accepted for Publication: April 6, 2010.

Author Contributions:Study concept and design: Ullman and Edlow. Acquisition of data: Ullman. Drafting of the manuscript: Ullman and Edlow. Critical revision of the manuscript for important intellectual content: Ullman and Edlow. Administrative, technical, and material support: Ullman. Study supervision: Edlow.

Financial Disclosure: None reported.

Edlow  JANewman-Toker  DESavitz  SI Diagnosis and initial management of cerebellar infarction. Lancet Neurol 2008;7 (10) 951- 964
PubMed
Strupp  MZingler  VCArbusow  V  et al.  Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. N Engl J Med 2004;351 (4) 354- 361
PubMed
Savitz  SICaplan  LREdlow  JA Pitfalls in the diagnosis of cerebellar infarction. Acad Emerg Med 2007;14 (1) 63- 68
PubMed
Halmagyi  GMCurthoys  IS A clinical sign of canal paresis. Arch Neurol 1988;45 (7) 737- 739
PubMed
Newman-Toker  DEKattah  JCAlvernia  JEWang  DZ Normal head impulse test differentiates acute cerebellar strokes from vestibular neuritis. Neurology 2008;70 (24, pt 2) 2378- 2385
PubMed
Cnyrim  CDNewman-Toker  DKarch  CBrandt  TStrupp  M Bedside differentiation of vestibular neuritis from central “vestibular pseudoneuritis.” J Neurol Neurosurg Psychiatry 2008;79 (4) 458- 460
PubMed
Kattah  JCTalkad  AVWang  DZHsieh  YHNewman-Toker  DE HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke 2009;40 (11) 3504- 3510
PubMed
Kerber  KABrown  DLLisabeth  LDSmith  MAMorgenstern  LB Stroke among patients with dizziness, vertigo, and imbalance in the emergency department: a population-based study. Stroke 2006;37 (10) 2484- 2487
PubMed
Lee  HSohn  SICho  YW  et al.  Cerebellar infarction presenting isolated vertigo: frequency and vascular topographical patterns. Neurology 2006;67 (7) 1178- 1183
PubMed

Figures

Place holder to copy figure label and caption
Figure.

Cardiac monitor showing sinus rhythm on arrival (A) and complete heart block immediately after the head impulse test (B).

Graphic Jump Location

Tables

References

Edlow  JANewman-Toker  DESavitz  SI Diagnosis and initial management of cerebellar infarction. Lancet Neurol 2008;7 (10) 951- 964
PubMed
Strupp  MZingler  VCArbusow  V  et al.  Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. N Engl J Med 2004;351 (4) 354- 361
PubMed
Savitz  SICaplan  LREdlow  JA Pitfalls in the diagnosis of cerebellar infarction. Acad Emerg Med 2007;14 (1) 63- 68
PubMed
Halmagyi  GMCurthoys  IS A clinical sign of canal paresis. Arch Neurol 1988;45 (7) 737- 739
PubMed
Newman-Toker  DEKattah  JCAlvernia  JEWang  DZ Normal head impulse test differentiates acute cerebellar strokes from vestibular neuritis. Neurology 2008;70 (24, pt 2) 2378- 2385
PubMed
Cnyrim  CDNewman-Toker  DKarch  CBrandt  TStrupp  M Bedside differentiation of vestibular neuritis from central “vestibular pseudoneuritis.” J Neurol Neurosurg Psychiatry 2008;79 (4) 458- 460
PubMed
Kattah  JCTalkad  AVWang  DZHsieh  YHNewman-Toker  DE HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke 2009;40 (11) 3504- 3510
PubMed
Kerber  KABrown  DLLisabeth  LDSmith  MAMorgenstern  LB Stroke among patients with dizziness, vertigo, and imbalance in the emergency department: a population-based study. Stroke 2006;37 (10) 2484- 2487
PubMed
Lee  HSohn  SICho  YW  et al.  Cerebellar infarction presenting isolated vertigo: frequency and vascular topographical patterns. Neurology 2006;67 (7) 1178- 1183
PubMed

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