Kindly provide detailed analysis with diagnosis patient is having continuous dizziness

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"Dizziness"[MeSH Terms]

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continuous dizziness evaluation red flags clinical guideline vestibular 2025

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site:acsearch.acr.org dizziness ataxia appropriateness criteria MRI 2025

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PMID: 41950225

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mkdir -p "/tmp/workspace/vng-analysis/output" && python -c "import pdfplumber; p='/tmp/workspace/attachments/3d568990-f586-4c04-aec7-20b56b30cfb3/Mohit Singh VNG 13 october.pdf'; pdf=pdfplumber.open(p); out=[]; [out.append('--- PAGE %d ---\n%s' % (i+1, (page.extract_text() or ''))) for i,page in enumerate(pdf.pages)]; open('/tmp/workspace/vng-analysis/output/extracted.txt','w',encoding='utf-8').write('\n\n'.join(out)); print('pages',len(pdf.pages)); print('\n\n'.join(out)[:12000])"

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python -c "import pdfplumber; p='/tmp/workspace/attachments/3d568990-f586-4c04-aec7-20b56b30cfb3/Mohit Singh VNG 13 october.pdf'; pdf=pdfplumber.open(p); [print('\n--- PAGE',i+1,'---\n'+(pdf.pages[i].extract_text() or '')) for i in range(14,len(pdf.pages))]"

Clinical interpretation of the VNG

Patient: Mr Mohit Singh Sisodiya, 33 years
Test date: 13 October 2026
Presenting symptom: continuous dizziness

Bottom-line impression

This VNG is not normal, but it does not provide a single definite diagnosis. The pattern is not typical of simple BPPV alone, and because the patient has continuous dizziness plus some vertical/positional eye-movement findings, a central neurological cause must be actively excluded by clinical examination.

Most appropriate working diagnosis:
Persistent dizziness with abnormal/atypical positional and oculomotor findings - possible central vestibular involvement versus atypical positional vestibular disorder.
This should be evaluated by an ENT neurotologist or neurologist, rather than treated as routine BPPV based only on this VNG.

Key findings in the report

VNG component	Report finding	Interpretation
Spontaneous nystagmus	None detected in light or dark	Reassuring, but does not rule out vestibular or central disease.
Gaze-evoked nystagmus	No meaningful horizontal gaze nystagmus with fixation	No clear gaze-holding abnormality recorded.
Saccades	Latency approximately 181-282 ms, with generally acceptable precision	No major clear saccadic abnormality evident from the raw values, though interpretation requires the laboratory's normal ranges.
Horizontal smooth pursuit	Low gains in some recordings, especially at 0.2 Hz	Could reflect poor tracking, fatigue, attention, visual factors, medication effect, or central ocular-motor dysfunction. It is not diagnostic by itself.
Vertical smooth pursuit	Marked asymmetry/low downward gain in the 0.2 Hz test	An abnormal or asymmetric vertical pursuit pattern deserves clinical correlation, particularly if there are neurological symptoms.
Optokinetic testing	Horizontal gains broadly symmetric and near expected range	Does not show a striking major optokinetic asymmetry.
Head-shake test	Vertical nystagmus recorded, slow-phase velocity about 35.8 degrees/s in one channel	Vertical nystagmus after head shaking is an atypical finding. Depending on tracing quality and examination, this may raise concern for central vestibular/cerebellar involvement, but it cannot establish that diagnosis alone.
Dix-Hallpike right	A small horizontal response while sitting; vertical response when supine/head-right	Does not show a straightforward classic posterior-canal BPPV pattern.
Dix-Hallpike left	Small mixed responses during supine/head-left, then a more prominent horizontal nystagmus on returning to sit, slow-phase velocity about 18.9 degrees/s	Positional response is present but the direction and sequence are not a clean, classic BPPV pattern from this raw report.
Yacovino maneuver	Vertical response during head extension, around 6 degrees/s	May indicate positional vestibular activation. However, isolated vertical positional nystagmus requires expert review because it may be atypical peripheral BPPV or, less commonly, central positional nystagmus.
Supine roll test, McClure-Pagnini	No clear nystagmus recorded	Makes horizontal-canal BPPV less likely on this examination.
Subjective visual vertical	Deviation only about 1 degree right/left	Essentially symmetrical and reassuring.
Caloric test / unilateral weakness	Not included in the supplied report	A major limitation. This report cannot determine whether one horizontal vestibular nerve/ear is weak without caloric or video head impulse results.

What the findings do and do not suggest

1. Classic posterior-canal BPPV is not strongly supported

BPPV usually causes brief attacks, typically under a minute, triggered by rolling in bed, looking up, lying down, or getting up. It should not usually cause an unremitting continuous dizziness all day.

The positional findings here are mixed and atypical. The VNG alone should not be used to label this as simple BPPV and repeatedly perform repositioning maneuvers without a bedside specialist assessment.

2. Vestibular neuritis is possible only if the clinical story fits

Vestibular neuritis typically causes sudden, severe continuous spinning vertigo for days, nausea, imbalance, and gradual improvement. It often leaves a unilateral vestibular deficit on caloric testing or video head-impulse testing. The necessary caloric data are absent here.

If dizziness has persisted for weeks to months without the acute onset pattern, vestibular neuritis becomes less likely as the complete explanation.

3. Central vestibular causes need exclusion

The following make specialist neurological assessment appropriate:

Persistent continuous dizziness rather than only brief triggered spells
Vertical nystagmus after head shaking
Vertical and atypical positional nystagmus
Potentially reduced/asymmetric smooth pursuit

These findings are not proof of stroke, tumor, multiple sclerosis, or cerebellar disease. They are reasons not to dismiss the symptoms as benign positional vertigo without a proper examination. In continuous acute vestibular syndrome, the main high-risk differential is vestibular neuritis versus posterior-circulation stroke. Rosen's Emergency Medicine: Concepts and Clinical Practice, p. 186.

A recent systematic review found that stroke risk among emergency-department dizziness presentations is clinically meaningful and supports standardized bedside examinations and selective neuroimaging in higher-risk cases, as summarized in this 2026 systematic review (PMID 41950225). The percentage in any individual patient cannot be inferred from that study or from this VNG.

Differential diagnosis, in order of practical concern

Central vestibular disorder to be excluded
- Cerebellar or brainstem process
- Demyelinating disease
- Less commonly migraine-related central vestibular dysfunction
- Risk rises if there are neurological symptoms, severe new headache, neck pain, vascular risks, or inability to walk independently.
Atypical positional vertigo / possible anterior-canal or non-classical BPPV
- The Yacovino/Dix-Hallpike findings could be positional, but the pattern should be reviewed directly by a neurotologist familiar with the tracings.
Vestibular migraine
- Common in younger adults and may cause persistent or recurrent dizziness, visual motion sensitivity, nausea, head-motion intolerance, and sometimes no headache during attacks.
- VNG can be normal or show nonspecific abnormalities. Diagnosis is clinical.
Persistent postural-perceptual dizziness (PPPD)
- Consider only if symptoms have lasted at least 3 months and are worse with standing, movement, visually busy settings, scrolling, crowds, or supermarkets.
- It can follow an initial vestibular event, migraine episode, or anxiety-related physiological sensitization.
- This is a real functional vestibular disorder, not “imagined dizziness,” but it is diagnosed after excluding important active vestibular and neurological conditions.
Peripheral vestibular hypofunction
- Needs caloric testing and/or video head impulse test to confirm or exclude. These results are not available in this report.
Non-vestibular contributors
- Orthostatic hypotension, dehydration, anemia, thyroid/glucose disorders, cardiac rhythm problems, medication or substance effects, visual problems, sleep deprivation, anxiety, and cervical issues. These require history, examination, and targeted testing.

Recommended next steps

Seek emergency assessment today if any of these are present

New weakness, numbness, facial droop, trouble speaking or swallowing
Double vision, new severe imbalance, inability to sit or walk without help
Severe or unusual headache
Neck pain after trauma or sudden neck pain with dizziness
New hearing loss in one ear
Repeated vomiting or inability to keep fluids down
Fainting, chest pain, palpitations, or shortness of breath
Sudden onset of continuous spinning dizziness within the last days, especially with vascular risks

A patient unable to stand unaided should have a central cause excluded. Tintinalli's Emergency Medicine: A Comprehensive Study Guide, p. 186.

Arrange an urgent outpatient review within days if no emergency red flags

With an ENT neurotologist or neurologist, bring the original VNG PDF. The clinician should perform:

Full neurological and cerebellar examination
Ear examination and audiogram
Bedside positional examination, ideally using video goggles
Careful assessment of gait and tandem gait
Orthostatic blood pressure and pulse
ECG if presyncope, palpitations, or cardiac symptoms
Medication and substance review
Video head impulse test and/or caloric vestibular testing, since caloric results are not in this report
Consider MRI brain with attention to posterior fossa/internal auditory canals if examination remains abnormal, symptoms are persistent/progressive, or central signs are found

For a true acute continuous vestibular syndrome with spontaneous nystagmus, a trained clinician may use the HINTS/HINTS-plus examination. It should not be self-performed or interpreted from VNG alone.

Symptom safety

Avoid driving, climbing, operating machinery, or working at height while continuously dizzy.
Maintain hydration and regular meals.
Use support when walking if unsteady.
Do not take long courses of vestibular suppressants such as meclizine, prochlorperazine, or benzodiazepines without clinician direction, because prolonged use can interfere with vestibular compensation.
Vestibular rehabilitation may be useful once dangerous central causes and the exact vestibular diagnosis have been assessed.

Final conclusion

The report demonstrates atypical positional/vertical nystagmus and possible oculomotor smooth-pursuit abnormalities, with no documented spontaneous nystagmus and no evidence in the report for horizontal-canal BPPV. It is not sufficient to diagnose a specific ear disorder, and the absent caloric/vHIT data are important limitations.

Given the complaint of continuous dizziness, the safest interpretation is: abnormal but non-localizing VNG, requiring neurotology/neurology evaluation to exclude a central cause before treating as BPPV.

Only hyperventilation induced nystgamus test found vertigo

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hyperventilation induced nystagmus vestibular systematic review

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hyperventilation induced nystagmus vestibular testing interpretation vestibular schwannoma review

If vertigo was provoked only during the hyperventilation test, that is important, but it is not diagnostic of one specific disease.

In the VNG report, hyperventilation produced a small vertical nystagmus response:

Right eye slow-phase velocity: 3.99 degrees/second
Left eye slow-phase velocity: 4.89 degrees/second
No spontaneous nystagmus was recorded at rest in light or dark.

What this can mean

Hyperventilation lowers carbon dioxide temporarily, which can alter nerve conduction and transiently uncover a subtle vestibular imbalance. It can provoke dizziness/nystagmus in:

Prior or compensated unilateral vestibular weakness, including after vestibular neuritis
Vestibular nerve disorders, including rarely vestibular schwannoma
Central demyelinating conditions, much less commonly
Physiological anxiety/hyperventilation response, especially if symptoms include tingling around the mouth/hands, chest tightness, trembling, or a feeling of panic

Textbook neurology sources state that hyperventilation-induced nystagmus can occur with vestibular schwannoma, following vestibular neuritis, or in central demyelinating lesions. Localization in Clinical Neurology, 8e, p. 2990. But this finding alone cannot diagnose any of these conditions.

Important correction to the practical interpretation

A mild hyperventilation-induced response, by itself, does not mean brain disease or tumor. In this report, there is no documented spontaneous nystagmus and no caloric test or video head-impulse result to show a definite ear-side vestibular weakness. Therefore, the VNG result should be termed:

Hyperventilation-induced nystagmus/vertigo, nonspecific. Clinical correlation and completion of vestibular testing are needed.

Best next steps

Audiometry/hearing test, especially if there is one-sided hearing reduction, tinnitus, ear fullness, or asymmetric hearing.
Caloric test and/or video head-impulse test (vHIT), because these assess unilateral vestibular weakness and are missing from the supplied VNG.
ENT neurotologist review if dizziness is persistent.
Consider MRI brain/internal auditory canals only if there is asymmetric sensorineural hearing loss, unilateral tinnitus, neurological signs, progressive symptoms, or an ENT/neurologist identifies concerning findings.

If the patient becomes dizzy specifically when breathing fast and has tingling, palpitations, chest tightness, or anxiety symptoms, dysfunctional breathing/hyperventilation may be contributing. That should still be assessed clinically rather than presumed to be the sole cause.

Seek urgent care if dizziness is accompanied by weakness, double vision, slurred speech, new severe headache, inability to walk independently, fainting, or sudden one-sided hearing loss.

Normal hearing with type A provide me the final report with diagnosis

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hyperventilation induced nystagmus vestibular

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hyperventilation induced nystagmus vestibular testing interpretation review

Final Vestibular Assessment Report

Patient: Mr Mohit Singh Sisodiya, 33 years
Presenting complaint: Continuous dizziness
Audiology: Hearing within normal limits bilaterally
Immittance: Type A tympanogram bilaterally, indicating normal middle-ear pressure and tympanic-membrane mobility.

VNG Summary

No spontaneous nystagmus detected in light or darkness.
No clinically significant gaze-evoked nystagmus noted.
Positional and Dix-Hallpike testing does not demonstrate a consistent classical BPPV pattern.
Supine roll testing is negative, with no evidence of horizontal-canal BPPV.
Subjective visual vertical is within normal limits.
Hyperventilation test provoked vertigo with nystagmus, recorded as a mild vertical response.
No caloric test or vHIT result is available in the supplied report. Therefore, the presence, side, and degree of peripheral vestibular weakness cannot be determined.

Impression

Positive hyperventilation-induced nystagmus with provoked vertigo.

In the setting of normal hearing and bilateral Type A tympanograms, this pattern is most consistent with a possible compensated peripheral vestibular dysfunction, potentially following a previous mild vestibular neuritis or transient vestibular imbalance.

Hyperventilation-induced nystagmus is a nonspecific vestibular sign. It may occur because hyperventilation temporarily changes nerve conduction and unmasks a compensated vestibular asymmetry. It does not independently establish a diagnosis of vestibular schwannoma, central neurological disease, or BPPV. Localization in Clinical Neurology, 8e, p. 2990.

Provisional Diagnosis

Probable compensated peripheral vestibulopathy with hyperventilation-induced nystagmus.
No evidence of BPPV or middle-ear pathology on the available tests.

Recommendations

ENT/neurotology consultation for clinical correlation.
Complete vestibular evaluation with bithermal caloric testing and/or video head impulse test (vHIT) to determine whether a unilateral vestibular hypofunction exists and, if present, which side is affected.
Vestibular rehabilitation therapy may be considered if imbalance or movement-related dizziness persists, after clinical assessment.
MRI of brain/internal auditory canals is not automatically required from this isolated mild finding with normal hearing. It should be considered if there is progressive persistent dizziness, unilateral tinnitus, new hearing asymmetry, neurological signs, severe headache, or abnormal neurological examination.

Clinical caution: Seek urgent medical assessment if dizziness occurs with weakness, numbness, double vision, difficulty speaking/swallowing, severe headache, fainting, inability to walk without support, or sudden hearing loss.

With full differential diagnosis provide the full detailed graph specific report.

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"Vestibular Migraine" AND vestibular testing

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Bárány Society diagnostic criteria persistent postural perceptual dizziness vestibular migraine 2025

Detailed VNG Interpretation Report

Patient: Mr Mohit Singh Sisodiya
Age/Sex: 33 years / Male
Test date: 13 October 2026
Clinical complaint: Continuous dizziness
Audiology: Hearing within normal limits bilaterally
Immittance: Bilateral Type A tympanograms, consistent with normal middle-ear pressure and mobility.

Key clinical clarification: Vertigo was reported only during the hyperventilation-induced nystagmus test. It was not provoked during routine positional or gaze testing.

1. Test-specific VNG findings

Test domain	Recorded result	Interpretation
Spontaneous nystagmus, light	Absent	No resting vestibular asymmetry detected under fixation.
Spontaneous nystagmus, dark	Absent	No clear spontaneous peripheral vestibular nystagmus unmasked without fixation.
Gaze testing with fixation	No nystagmus	No gaze-evoked nystagmus identified.
Gaze testing without fixation	Very low-amplitude intermittent vertical signals, approximately 2.0-2.6 degrees/s in eccentric gaze	Mild, nonspecific finding. It requires correlation with the actual VNG tracing, calibration, alertness, and eye-blink artifact. It is not diagnostic of central disease by itself.
Saccades	Latency approximately 181-282 ms; precision broadly preserved	No definite major saccadic abnormality apparent from the supplied values.
Smooth pursuit	Variable and reduced gains, especially at low frequency and in vertical tracking	Nonspecific. Can arise from attention, fatigue, medications, poor visual tracking, calibration, or central ocular-motor causes. It should not be interpreted in isolation.
Optokinetic nystagmus	Horizontal gain broadly symmetric, approximately 0.93-1.05	No clear clinically significant optokinetic asymmetry.
Head-shake test	A vertical response recorded	No symptom provocation reported. A vertical response requires tracing review but is not sufficient to establish a diagnosis without clinical examination.
Dix-Hallpike, right	Minor/variable recorded eye movements; no typical sustained torsional-upbeating posterior-canal BPPV pattern	Negative for definite right posterior-canal BPPV.
Dix-Hallpike, left	Minor/variable positional signals; no consistent classical BPPV pattern	Negative for definite left posterior-canal BPPV.
Yacovino positional test	Small vertical response during head extension, but no reported vertigo	Atypical, nonspecific positional response. Does not establish anterior-canal BPPV.
Supine roll, McClure-Pagnini	No nystagmus	No evidence of horizontal-canal BPPV.
Subjective visual vertical	Approximately 1 degree deviation	Within expected normal limits and does not suggest a major otolith imbalance.
Hyperventilation test	Vertigo reproduced; small vertical nystagmus, slow-phase velocity about 4.0-4.9 degrees/s	Positive hyperventilation-induced nystagmus with symptom provocation.
Caloric irrigation / unilateral weakness	Not available in report	Cannot determine whether there is unilateral vestibular hypofunction, or identify an involved side.
vHIT	Not available	Semicircular-canal vestibulo-ocular reflex function not assessed.

2. Graph-specific clinical correlation

The VNG graphs show the following practical pattern:

Resting nystagmus      [Normal / absent]
Gaze nystagmus         [No significant abnormality]
Saccades               [No definite major abnormality]
Optokinetic response   [Broadly symmetric]
Positional testing     [No diagnostic BPPV pattern]
Supine roll test       [Negative]
SVV / otolith screen   [Normal]
Hyperventilation       [Vertigo + mild induced vertical nystagmus]
Caloric / vHIT         [Not performed or not supplied]

Interpretation of the pattern

No hearing loss + Type A tympanograms
                  ↓
No evidence of middle-ear disorder

No spontaneous nystagmus + negative roll test + no classical Dix-Hallpike pattern
                  ↓
No objective evidence of active classic BPPV or acute uncompensated peripheral vestibular loss

Hyperventilation produces vertigo and nystagmus
                  ↓
Suggests an inducible vestibular imbalance, but does not localize the side or determine a specific diagnosis

Diagnostic Impression

Provisional vestibular diagnosis

Hyperventilation-induced vertigo with mild hyperventilation-induced nystagmus, in the setting of normal hearing and normal middle-ear function.

No objective VNG evidence of classical posterior-canal or horizontal-canal BPPV.

No clear evidence of an acute uncompensated peripheral vestibular lesion on the available VNG data.

The most appropriate report conclusion is:

Nonspecific positive hyperventilation test, suggestive of possible compensated vestibular dysfunction or heightened vestibular sensitivity. Further vestibular and clinical evaluation is required before assigning a definitive peripheral or central diagnosis.

Hyperventilation decreases carbon dioxide and produces transient alkalosis, which can alter neural excitability and may unmask a previously compensated vestibular asymmetry. Localization in Clinical Neurology, 8e, p. 2990.

Differential Diagnosis

A. More plausible considerations

1. Compensated unilateral peripheral vestibular hypofunction

Possibility: moderate

This can occur after a previous mild vestibular neuritis, labyrinthine insult, viral illness, or an episode of acute vertigo that has partially recovered. A patient may have no spontaneous nystagmus once compensation has occurred but may show symptoms with provocative tests such as hyperventilation.

Supporting features

Vertigo provoked by hyperventilation
No active resting nystagmus, compatible with compensation
Normal hearing does not exclude vestibular neuritis

Missing confirmation

Caloric test
vHIT
Vestibular evoked myogenic potentials, if indicated

2. Dysfunctional breathing / hyperventilation-related dizziness

Possibility: moderate to high if symptoms occur during anxiety, rapid breathing, stress, exertion, or panic

Hyperventilation can independently cause dizziness, light-headedness, unreality, visual blurring, tingling around the mouth/hands, chest tightness, shakiness, and palpitations. It may also trigger mild ocular-motor responses in a susceptible person.

Supporting features

Vertigo occurs only during deliberate hyperventilation in the test
No confirmed caloric weakness or BPPV pattern
Normal hearing and Type A tympanograms

Clinical question Ask whether episodes outside the test occur with rapid breathing, stress, panic, pain, crowded places, exercise, or poor sleep.

3. Vestibular migraine

Possibility: moderate, depending on history

Vestibular migraine can cause dizziness or vertigo with normal hearing and often nondiagnostic VNG findings. Symptoms may be spontaneous, motion-induced, visually induced, or position-related. Headache may be absent during some vestibular attacks.

Supporting features if present clinically

Past or family history of migraine
Motion sensitivity
Light or sound sensitivity
Nausea
Visual aura
Symptoms triggered by poor sleep, skipped meals, stress, dehydration, menstruation, or certain foods

Important limitation VNG does not diagnose vestibular migraine. It is a clinical diagnosis after appropriate exclusion of competing disorders.

4. Persistent postural-perceptual dizziness, PPPD

Possibility: consider if symptoms have persisted for 3 months or more

PPPD produces chronic non-spinning dizziness, swaying, rocking, imbalance, or a floating sensation. It typically worsens when upright, moving, using screens, walking in supermarkets, riding in vehicles, or watching visually busy scenes.

Supporting features if present clinically

Symptoms on most days for at least 3 months
Worse with standing, walking, movement, scrolling, crowds, traffic, or supermarket aisles
Began after vestibular illness, migraine, stressful event, or panic episode

PPPD is a chronic functional vestibular disorder, not a structural ear disease. Harrison’s Principles of Internal Medicine, 22e, functional dizziness section.

B. Conditions requiring targeted exclusion

5. Vestibular paroxysmia

Possibility: low unless episodes are very brief, frequent, and stereotyped

This condition usually produces many short, recurrent episodes, often lasting seconds to minutes, not continuous all-day dizziness. Hyperventilation can occasionally provoke nystagmus in vestibular-nerve disorders, but the clinical pattern is more important than the VNG alone.

Consider only if there are repeated short attacks, sometimes with unilateral ear symptoms such as tinnitus or ear pressure.

6. Vestibular schwannoma or other eighth-nerve lesion

Possibility: low with normal hearing, but not zero

Hyperventilation-induced nystagmus can occur in vestibular schwannoma. However, it is not diagnostic, and vestibular schwannoma more often has asymmetric sensorineural hearing loss, unilateral tinnitus, or abnormal unilateral vestibular testing.

Current status: Normal bilateral hearing reduces the likelihood. MRI is not automatically required solely due to this VNG response, but it may be appropriate if symptoms are progressive or a specialist finds asymmetry/neurological abnormalities.

7. Central vestibular or neurological disorder

Possibility: low based on the supplied data, but clinical examination remains essential

The VNG does not demonstrate a clear central pattern. Small vertical signals during hyperventilation or positional testing can be nonspecific and may be technical or physiological. Still, persistent dizziness needs neurological review if there are red flags.

Consider central causes such as cerebellar/brainstem pathology, demyelination, or other neurological disorders if there is:

Persistent severe imbalance or inability to walk unaided
Double vision, slurred speech, weakness, numbness, facial asymmetry, swallowing difficulty
Severe new headache or neck pain
Direction-changing gaze-evoked nystagmus
Persistent downbeat or pure vertical spontaneous nystagmus
Progressive symptoms

C. Less likely based on current data

Disorder	Why less likely on available findings
Posterior-canal BPPV	No consistent classic positional torsional-upbeating nystagmus; vertigo not provoked on Dix-Hallpike.
Horizontal-canal BPPV	Supine roll test is negative.
Ménière disease	Normal hearing and no documented fluctuating hearing loss, episodic aural fullness, or tinnitus.
Acute labyrinthitis	Usually associated with acute vertigo and hearing loss.
Acute vestibular neuritis	Usually causes an acute sustained severe vertigo syndrome with spontaneous unidirectional nystagmus early in the illness. A prior compensated episode remains possible.
Middle-ear disease	Type A tympanograms and normal hearing make this unlikely.

Final Report Wording

Impression: Audiological evaluation reveals normal bilateral hearing sensitivity with bilateral Type A tympanograms, consistent with normal middle-ear function. VNG demonstrates no spontaneous or clinically significant gaze-evoked nystagmus. Positional testing does not reveal a reproducible classical pattern of posterior- or horizontal-canal BPPV. Subjective visual vertical is within normal limits. Hyperventilation provokes vertigo associated with a mild induced vertical nystagmus response.

Conclusion: Positive, nonspecific hyperventilation-induced nystagmus/vertigo. Findings may reflect a compensated peripheral vestibular imbalance, vestibular hypersensitivity, or a hyperventilation-related physiological response. No definitive side-specific peripheral vestibular lesion can be diagnosed because caloric testing and vHIT results are unavailable. Clinical correlation by an ENT neurotologist or neurologist is advised.

Recommended Next Investigations

Bithermal caloric test
To assess low-frequency function of each horizontal semicircular canal and detect unilateral weakness.
Video head impulse test, vHIT
To examine high-frequency vestibulo-ocular reflex function in all semicircular canals.
Bedside neurological and vestibular examination
Including gait, tandem gait, eye movements, head-impulse test, skew deviation, positional maneuvers, and orthostatic blood pressure.
Screen for migraine and PPPD features
This may identify vestibular migraine or persistent postural-perceptual dizziness when vestibular tests are otherwise non-localizing.
MRI brain and internal auditory canals with contrast only if clinically indicated
Consider if unilateral tinnitus, asymmetric hearing, progressive neurological symptoms, persistent unexplained imbalance, or abnormal specialist examination is present.
Vestibular rehabilitation therapy
Consider after the clinical assessment if there is movement sensitivity, imbalance, or suspected compensated peripheral dysfunction.

Urgent referral indicators

Urgent emergency assessment is needed for new weakness/numbness, double vision, speech or swallowing difficulty, severe headache, fainting, chest pain, inability to walk without assistance, sudden one-sided hearing loss, or rapidly worsening symptoms.

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