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Detailed history essential to diagnosis of the dizzy patient
Onset date, duration, frequency, context, triggers, aggravating or alleviating factors, and any associated signs or symptoms are important.
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Dizziness is a term used to describe a variety of symptomatology including lightheadedness, presyncope, imbalance and spinning of the environment known as vertigo.
While the majority of acute dizziness cases will present to the emergency department, the eye care provider may be consulted to evaluate for ocular pathology and, in some cases, may be the first to encounter it.
Case report
A 50-year-old Caucasian man presented for an ocular examination with the complaint of periodic dizziness and horizontal, binocular diplopia in extreme right gaze for 2 months. Ocular history revealed presbyopia in both eyes. Medical history included allergic rhinitis, childhood asthma, depression, insomnia and vitamin D deficiency. Medications included Klonopin (clonazepam, Genentech), Antivert (meclizine, Pfizer), Centrum OTC (Wyeth Consumer Healthcare), Nicoderm CQ (nicotine patch, GSK) and Caltrate (vitamin D3, Pfizer). He had no known drug allergies. Family history was positive for diabetes, heart disease, hypertension and lung cancer. Social history was positive for tobacco dependence; he denied alcohol or illicit drug use.
Best corrected visual acuities were 20/20 OD and 20/20 OS. Pupils were normal without afferent pupillary defect. Extraocular muscles revealed gaze-evoked and tortional nystagmus as well as a right horizontal gaze palsy. Visual fields showed superior defects extending from the blind spot of the right eye and extension of the blind spot of the left eye. Cover test was orthophoric at distance and six exophoria at near. Ishihara color vision was reduced at 0/12 OD and 2/12 OS. Anterior segment examination was normal. Goldmann applanation tonometry was 19 mm Hg OD and 17 mm Hg OS. Angles were open gonioscopically in the right and left eyes. Posterior segment examination revealed trace temporal pallor of the optic nerve heads bilaterally; the cup-to-disc ratio measured 0.30 x 0.30 OD and 0.50 x 0.50 OS. All other findings were normal. Spectralis OCT (Heidelberg) of the retinal nerve fiber layer (RNFL) showed abnormal thinning of the inferior-temporal RNFL, borderline thinning temporally in the right eye and borderline generalized thinning in the left eye.
The patient presented to the emergency department for immediate neurology evaluation and testing. MRI of the head and orbits with and without contrast revealed periventricular white matter, pontomedullary junction and brainstem demyelinating lesions. Spinal MRI revealed multiple abnormal T2 foci within the thoracic region. Lumbar puncture and cerebrospinal fluid analysis revealed positive oligoclonal banding. Complete blood count with differential, CMP, Westergren ESR, CRP, ANA, FTA-ABS, RPR, vitamin B12, folate, homocysteine, MMA, NMO antibody, JC virus and lipid panel were normal or negative.
Clinical findings of dizziness, gaze palsy and nystagmus correlated with brain lesions caused by multiple sclerosis (MS). Bilateral optic atrophy was attributed to previous asymptomatic episodes of demyelinating optic neuritis and/or active MS-associated accelerated RNFL loss.
The patient was started on Tysabri (natalizumab, Biogen) and referred for physical, occupational and speech therapy. Smoking cessation counseling was provided. Dizziness and eye movement abnormalities improved significantly with treatment; the optic atrophy remained stable.
Humphrey visual field 30-2 SITA Standard demonstrating superior defects extending from the blind spot of the right eye (left) and extension of the blind spot of the left eye (right).
Images: Porzukowiak TR and Koh LV
The historical approach to the dizzy patient involved the practitioner asking: “What do you mean by dizzy?” If the patient responded by saying spinning or a motion implying vertigo, a search for a vestibular cause was evaluated. If the patient said he or she was becoming faint or experiencing presyncope, a cardiovascular disease was sought. In the case of disequilibrium or unsteady gait, a neurologic etiology was most concerning. Nonspecific dizziness or any other dizziness sensation led to a search for a psychiatric or metabolic cause.
Triage, timing, triggers, telltale signs
Newer approaches to the dizzy patient popularized by neurologist David E. Newman-Toker, MD, PhD, of Johns Hopkins University School of Medicine, focus on triage, timing, triggers and telltale signs in a search for an accurate diagnosis.
Triage involves focusing on clinical red flags that immediately point to a serious cause of dizziness requiring emergent evaluation as outlined in the accompanying table. Abnormalities of vital signs or mental state may be manifestations of addisonian crisis, anemia, carbon dioxide poisoning, decompression sickness, herpes simplex virus encephalitis, hypercapnia, hypoglycemia, hypoxia, hypotension, isoniazid intoxication, mountain sickness, myxedema, subdural hematoma, thyroid storm or Wernicke’s syndrome.
Pain, depending on location (abdomen, back, chest, ear, head, neck), may be a harbinger of abscess, carbon monoxide poisoning, carotid or vertebral dissection, giant cell arteritis, herpes zoster, intracranial hemorrhage, intracranial pressure abnormality, malignant otitis externa, mastoiditis, meningitis, myocardial infarction (MI), otitis media, pituitary apoplexy, pneumonia, pulmonary embolism (PE), spinal cord compression, thoracic/abdominal aortic aneurysm or dissection. Finally, neurologic or cardiovascular symptoms should prompt an emergent neurologic or cardiac evaluation, respectively.
The remainder of patients not exhibiting emergent red flag symptomatology are further divided by the timing of dizziness as transient/episodic (lasting seconds to hours) or persistent/continuous (lasting days to weeks).
Transient/episodic dizziness is more commonly benign in nature and may include benign paroxysmal positional vertigo, benign orthostatic hypotension, Meniere’s disease, panic attack, reflex syncope or vestibular migraine. The provider should be cautioned that more dangerous mimics of benign causes presenting as transient/episodic dizziness include cardiac arrhythmia, cardiovascular emergencies (e.g., MI, aortic dissection, PE and occult GI bleed), neuro-humoral neoplasm (e.g., insulinoma, pheochromocytoma), transient ischemic attack and toxic exposure (e.g., carbon monoxide). Persistent/continuous dizziness etiologies of the more common, benign nature include drug toxicity (e.g., anticonvulsants), herpes zoster oticus, vestibular neuritis or viral neuritis.
Spectralis OCT of the right eye demonstrating abnormal thinning of the inferior-temporal RNFL and borderline thinning temporally (left); the left eye exhibits borderline generalized thinning (right).
The provider should be cautioned to exclude the dangerous mimics that may also present with persistent/continuous dizziness, including bacterial labyrinthitis/mastoiditis; brainstem encephalitis (e.g., Listeria, herpes simplex) or Miller Fisher syndrome; brainstem, cerebellar or labyrinthine stroke; or Wernicke’s syndrome.
For patients with transient dizziness of less than 24 hours’ duration, a detailed history and exploration for triggers will help to further elucidate an etiology. In general, transient dizziness that is exertional and spontaneous, or untriggered, is most likely related to a dangerous cause. A trigger such as a change in head position is more likely related to a benign cause and may be replicated on physical exam (e.g., Dix-Hallpike’s maneuver).
For those cases with persistent dizziness greater than 24 hours, a neurologic examination with attention to the vestibulo-ocular reflex responses, ocular alignment and the presence or absence of nystagmus is necessary, as these patients are at high risk for stroke.
The eye care provider’s role
When a patient presents with dizziness to the primary eye care provider, a detailed history is critical, with questions pertaining to the dizziness red flags. Onset date, duration, frequency, context, triggers, aggravating or alleviating factors, and any associated signs or symptoms are important.
The ocular examination should focus on the cover test and extraocular muscle findings, looking for evidence of smooth pursuit, saccadic, cranial nerve, nystagmus or saccadic intrusion abnormality. Additional optokinetic nystagmus, Halmagyi head thrust maneuver, oculocephalic response (e.g., Doll’s eye maneuver), Dix-Hallpike’s maneuver, cranial nerve screen and gait assessment tests are helpful in isolating where in the brain a problem is most likely. Physical examination may also include blood pressure measurement (sitting and supine), heart rate and temperature. Communication of the ophthalmic findings to other medical specialists is important in the differential diagnosis of dizziness.
- References:
- Jensen JM. Vertigo and dizziness. In: Weiner WJ, Goetz CG, eds. Neurology for the Non-Neurologist. Philadelphia, PA: Lippincott, Williams, & Wilkins; 1999:205-219.
- Kerber KA, et al. Neurol Clin Pract. 2011;doi:10.1212/CPJ.0b013e31823d07b6.
- Newman-Toker DE. A new approach to the dizzy patient. Paper presented at: North American Neuro-ophthalmology Society; February, 2015; Coronado, CA.
- For more information:
- Len V. Koh, PhD, OD, MBA, FAAO, is assistant dean of clinical affairs and associate professor at Midwestern University, Glendale, Ariz. He can be reached at lkoh@midwestern.edu.
- Tina Renae Porzukowiak, OD, FAAO, is an associate professor at Midwestern University. She can be reached at tporzu@midwestern.edu.
Disclosure: Porzukowiak and Koh report no relevant financial disclosures.