Dizziness and Vertigo

Basic Anatomy
  • The vestibular system provides input to the brain regarding movement of the head. The vestibular portion of the 8th cranial nerve is composed of the utricle, the succulent, and three semicircular canals that lie at right angles to each other.
  • Maintenance of equilibrium is dependent upon input from the vestibular system and the eyes, as well as proprioception; in addition, the information must be properly integrated in the brain. Abnormal information, or improper integration, results in a complaint of "dizziness" or vertigo.
Scope of the Problem
  • The complaint of "dizziness" can be attributed to numerous disorders, both benign and life-threatening. The first task is to define the patient’s symptoms. Is it dizziness, vertigo or weakness? For patients with true vertigo, the next task is to determine the source of the symptoms; is it a peripheral or central vestibular process?
  • Peripheral vestibular disorders involve structures at the level of the inner ear and the 8th cranial nerve. Central lesions involve the vestibular nuclei (located in the brainstem) and their connections (e.g., CN III and VI nuclei, MLF).
Etiology
  • Peripheral Vestibular Disorders
    • Cerebellopontine angle tumor (e.g., meningioma, schwannoma)
    • Acute Ramsay Hunt syndrome
    • Benign paroxysmal positional vertigo (BPPV)
    • Acute vestibular neuronitis/neuritis or labyrinthitis
    • Perilymphatic fistula
    • Post-traumatic vertigo
    • Labyrinthine concussion
    • Meniere’s disease
  • Central Vestibular Disorders
    • Posterior fossa tumor
    • Vertebrobasilar ischemia/infarction
    • Multiple sclerosis
    • Cerebellar hemorrhage
    • Infections and parainfectious encephalomyelitis
    • Wernicke’s encephalopathy
Diagnosis
History
  • Ask the patient to describe the symptoms as accurately as possible: is there a spinning sensation (i.e., true vertigo); a sense of being off balance, without spinning (dysequilibrium); a faint feeling (near syncope); or an otherwise vague sensation of "lightheadedness?" Patients with vestibular lesions use decriptors such as spinning, feeling drunk or motion sick, or a sensation of imbalance (i.e., falling or tilting to one side). Patients with nonvestibular lesions explain the feeling as one of spinning inside the head, near-faint, floating, swimming in the head, or giddiness.
  • Determine the duration of the attack—seconds, minutes, or hours to days? Peripheral vestibular disorders are associated with intermittent episodes of vertigo that are sudden, brief, and severe; symptoms from central lesions have a more gradual onset, last longer, and are less intense.
  • Are the episodes provoked by specific movements, position changes, or maneuvers? Peripheral lesions are commonly initiated by turning the head to the side or tilting the head up, whereas central causes are not positional. Symptoms of vertebrobasilar insufficiency may be reproduced with neck movement. Valsalva’s maneuver worsens vertigo associated with a perilymphatic fistula. Symptoms that are precipitated by stress or certain situations (e.g., driving a car) generally indicate a nonvestibular cause. Cervical vertigo refers to the symptom complex of neck pain, vertigo, and nystagmus that is worse with movement of the neck.
  • Are there associated symptoms? Peripheral vestibular lesions are commonly associated with nausea or vomiting; hearing loss, tinnitus, or ear fullness; other neurologic deficits (e.g., diplopia, dysphagia, dysarthria, extremity weakness, or sensory impairment) almost always accompany a central lesion. Are there symptoms in the absence of vertigo? Loss of coordination between attacks indicates 8th cranial nerve or brainstem disease.
  • Has there been a recent illness? Vestibular neuritis and acute labyrinthitis are commonly preceded by a viral illness. Is there any history of trauma? Post-traumatic positional vertigo, labyrinthine concussion, and perilymphatic fistula are all caused by head trauma. A rapid, twisting injury of the neck can cause vertebral artery dissection or occlusion.
  • Does the patient’s medical history suggest an etiology? Uremia, Parkinson’s disease, diabetes, and chronic alcohol abuse are causes of peripheral neuropathy and orthostasis. Is the patient taking any medications that may cause orthostatic hypotension (e.g., diuretics, anti-hypertensives) or dysequilibrium (e.g., anti-convulsants, sedatives)? Is the patient on any new medications? Frequently, elderly patients with poor vision and sensation— especially after starting sedating medications—describe a feeling of being off balance and stumbling (dysequilibrium), without true vertigo or presyncopal symptoms.
  • Is there a history of similar episodes? What type of work-up was done, and what were the results? Patients with ill-defined light-headedness often have extensive work-ups without an explanation for their symptoms.
  • Is there a family history (e.g., spinocerebellar degeneration, Friedrich’s ataxia, ataxia-teloangiectasia, Wilson’s disease)?
Physical Exam
  • HEENT: Note any signs of trauma. Inspect the ears for evidence of infection, trauma, or cerumen impaction. Are there vesicles (suggestive of VZV); is there fluid or a TM perforation? With the patient looking straight forward, ensure that the eyes are properly aligned. Funduscopic exam may reveal papilledema, suggesting increased intracranial pressure from a mass lesion (usually in the posterior fossa).
  • Neck: evaluate range of motion; carotid bruits suggest atherosclerosis.
  • Cardiac exam: evaluate the rhythm and listen for murmurs (may suggest an outflow obstruction).
  • Neurologic Exam
    • Determine the patient’s mental status.
    • Abnormal cranial nerve findings suggest a central process.
      • Evaluate the extraocular muscles in all six cardinal positions of gaze and look for nystagmus. Nystagmus is described by the position of gaze in which it is provoked and the direction of the fast component. Nystagmus associated with peripheral disorders is generally horizontal or rotatory and does not change directions, but is more pronounced when the patient looks in the direction of the fast component (away from the involved side).
      • Central disorders produce gaze pareses and nystagmus in any direction (including vertical) that may change direction if the patient looks away from the direction of the fast phase.
      • Check the patient’s auditory acuity; perform Weber and Rinne tests.
      • If indicated by the history, test facial nerve function. The patient with a cerebellopontine angle tumor may have a depressed corneal reflex or facial nerve palsy ipsilateral to the lesion.
      • Lower brainstem disease may be accompanied by weakness of the tongue (CN XII), hoarseness, dysphagia, and weakness of the palate (CN IX and X).
    • Motor exam: Note any motor weakness or involuntary movements (e.g., asterixis, myoclonus, chorea).
    • Sensory exam: Proprioception and vibratory sensation are impaired in patients with sensory ataxia produced by neurosyphilis, vitamin B12 deficiency, and polyneuropathies.
    • Cerebellar exam: Tests of motor coordination evaluate cerebellar hemispheric function. These include finger-to-nose, finger-tapping and toe tapping, rapid alternating movements, and heel-knee-shin.
    • Stance: Romberg’s sign is positive if the patient is unable to stand with the feet together when the eyes are closed. This indicates a sensory (proprioceptive) or vestibular disorder. Patients with vestibular lesions will fall toward the side of the lesion. In contrast, patients with cerebellar pathology are unable to compensate with visual cues and are unsteady with eyes open or closed.
    • Gait: A wide-based, staggering gait is noted in cerebellar ataxia; in addition, tandem gait is always impaired.
    • Reflexes: hypoactive reflexes accompany cerebellar disorders and polyneuropathies causing sensory ataxia. Multiple sclerosis, vitamin B12 deficiency, and focal brainstem lesions are associated with hyperactive reflexes and the Babinski sign.
    • Dix-Hallpike maneuver: The seated patient is rapidly lowered onto the exam table with the head hanging off the end at a 20-degree angle. Ask the patient if he has vertigo and examine the patient’s eyes. Slowly return the patient to a sitting position and repeat the procedure with the head turned 45 degrees horizontally. Slowly return the patient to sitting with the head still at a 45-degree angle; repeat the procedure with the head turned to the other side.
    • Nystagmus associated with a peripheral vestibular disorder has a latency period (i.e., begins several seconds after the position change); fatigues (i.e., terminates spontaneously if the position is maintained); habituates (i.e., repeated maneuvers will result in less pronounced symptoms); and is suppressed when the gaze is fixed. In contrast, central vertigo is typically not positional, has no latency period, does not fatigue or habituate, and is not suppressed by visual fixation.
Ancillary Evaluation
  • Consider pulse oximetry when a systemic process is likely; in addition, patients with a history of trauma, possible stroke, or intracranial hemorrhage (ICH) may be hypoxic.
  • A bedside glucose test should be performed on all patients with neurologic symptoms.
  • Serum drug levels may be useful in patients on vertigogenic medications. Consider a toxicology screen in the appropriate clinical setting.
  • Patients with dizziness or ill-defined symptoms may require further evaluation with a complete blood count, electrolytes and other laboratories as indicated.
  • Emergent noncontrast CT scan of the head is indicated in patients with a suspected life-threatening central process (e.g., cerebellar hemorrhage, tumor, abscess, infarction). CT may also reveal bony erosion in cases of bacterial otomastoiditis with labyrinthine involvement.
  • MRI is indicated in patients suspected of having multiple sclerosis, posterior fossa tumor, or brainstem infarction (after negative head CT).
Differential Diagnosis
  • Syncope and near-syncope
  • Hypovolemia from any cause
  • Acute coronary syndrome
  • Intoxication
  • Hyperventilation syndrome
  • Anxiety and affective disorder
  • Dysequalibrium
  • Metabolic disorders
  • Sepsis
  • Intracranial pressure
Treatment
  • Peripheral Vestibular Disorders
    • Vestibular suppressants are useful in the acute period. Prolonged use may impede central compensation. Therefore, only a three-day supply should be prescribed (Table 4F.1).
    • Vestibular exercises facilitate the central compensation process and may be useful for patients with chronic vertigo or recurring BPPV. The patient should assume a position with his head that causes nystagmus, and then attempt to focus the eyes and move them in a position that maximizes his symptoms. As the nystagmus diminishes, the patient should begin to move the head up and down or from side to side while visually fixating on a target. He should attempt to stand and walk while the nystagmus is still present, and (as symptoms improve) should move the head from side to side or up and down while walking (first slowly, then quickly in all directions). Compensation may take several months.
    • Specific treatment
      • The Canalith repositioning maneuver is effective in cases of BPPV resulting from otoconia. Details of this procedure are described elsewhere. Note that patients may have an increase of symptoms as a result of repositioning maneuvers.

        Treatment options in peripheral vertigo
        Antihistamines Meclizine
        Diphenhydramine        		 25 mg PO q6h
        25-50 mg PO q6h
        Phenothiazines Prochlorperazine
        Promethazine        		 5-10 mg PO q6-8h; 25 mg PR q12h
        25-50 mg PO/IM q4-6h;
        Anticholinergics Scopolamine 0.5 mg transdermally q 3 days
        0.4-0.8 mg PO q6-8h
        Benzodiazepines Diazepam 5-10 mg PO q6-8h
        Serotonin antagonists Ondansetron 4 mg PO q 8 h

        Furthermore, feasibility of patient education in a busy ED may be an issue. Otolaryngology follow-up is advised.

      • Acute peripheral vestibulopathy encompasses vestibular neuritis and acute labyrinthitis of unknown etiology (but commonly preceded by a viral infection). Both disorders are associated with acute onset vertigo and nystagmus, nausea, and vomiting that may last for 2 wk. The distinction between the two is based on the presence (labyrinthitis) or absence (neuritis) of concomitant hearing loss or tinntus. A 3-day course of a vestibulosuppressant with bed rest is recommended. In addition, a 10-day course of prednisone may shorten the course of the illness.
      • Ramsay Hunt syndrome is a reactivation of varicella-zoster that can involve multiple cranial nerves (including V, VII, VIII, IX and X). Prednisone and acyclovir have been found to facilitate recovery, if treatment is initiated within 3 days (compared to more than 7 days) after symptom onset.
        • Prednisone 60 mg PO q day, tapered over 10 days
        • Acyclovir 400 mg PO 5x/day for 10 days
      • Meniere’s disease is thought to be caused by excessive fluid within the inner ear. It is characterized by acute attacks of vertigo and ear pressure lasting hours, associated with tinnitus and sensorineural hearing loss. In addition to vestibulosuppressants, patients may benefit from restricted sodium, caffeine, and nicotine intake. All patients with Meniere’s disease should be referred to ENT.
      • The patient with dysequilibrium caused by multiple sensory deficits functions better with improved lighting, elimination of sedating medications, and (in the short term) using a walker. He may benefit from a referral for vision refraction or rehabilitation, as indicated by his deficits.
Disposition
  • Patients with neurologic deficits or suspected central disorders should be admitted. Patients with intractable vomiting or severe dehydration may require inpatient treatment.
  • Patients with suspected peripheral vestibular disorders who are discharged home with medication should be instructed to follow-up with their PCP if symptoms persist more than a few days.
Suggested Reading
  1. Baloh RW. Dizziness: Neurological emergencies. Neurol Clin North Am 1998; 16:2.
  2. Disorders of equilibrium. In: Simon RP, Aminoff MJ, Greenberg DA, eds. Clinical Neurology 4th ed. Stamford: Appleton and Lange, 1999.
  3. Herr RD. Dizziness and vertigo. In: Howell JM, ed. Emergency Medicine. Philadelphia: WB Saunders Company, 1998.
  4. Tusa RJ. Vertigo. Neurol Clin 2001; 19:1.
       
eXTReMe Tracker