CNS Causes of Vertigo Clinical Presentation

Updated: May 03, 2017
  • Author: Marcelo B Antunes, MD; Chief Editor: Arlen D Meyers, MD, MBA  more...
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The history is of critical importance to determine if the vertigo is from a peripheral or central origin because usually physical findings and vestibular testing can only provide supportive information. Peripheral vertigo could be positional, lasting for seconds to a few minutes (such as in benign paroxysmal positional vertigo); recurrent, lasting for hours and associated with hearing loss, aural fullness, and tinnitus (such as in Meniere syndrome), [3] or a single episode lasting days without associated auditory or neurological symptoms (such as in vestibular neuronitis).

Central vertigo should be considered when the patient’s history is not consistent with any of the well-defined peripheral syndromes. The history could be acute or chronic vertigo, usually associated with neurologic symptoms. The presence of neurologic symptoms such as headaches, aura, visual, sensory or motor symptoms is more suggestive of a central disorder. [4, 5, 6]



The physical examination should also focus on findings that are consistent with either peripheral or central vestibular disorders. Findings suggestive of peripheral vestibular dysfunction include a positive head thrust test indicative of an abnormal vestibuloocular reflex (VOR), turning greater than 45° on the Fukuda stepping test, ability to perform tandem gait testing with eyes open but not closed, or a positive Dix-Halpike maneuver suggestive of benign positional vertigo (BPV).

Findings suggestive of central pathology are abnormalities on the neurologic examination such as diplopia, dysarthria, aphasia, weakness, and sensation abnormalities.

Signs of a cerebellar dysfunction such as dysmetria on finger-to-nose testing and dysdiadochokinesia are also characteristic of a central problem. [6, 7]

One of the most helpful tools during physical examination is an evaluation of any nystagmus. Nystagmus is be defined as a repetitive involuntary movement of the eyes. This is initiated by the slow phase, which is generated by the underlying disorder. The slow phase takes the eye away from the preferred position, and the fast phase (or saccade) brings the eye back to the visual target. The direction of the fast phase describes the direction of the nystagmus; the velocity of the nystagmus is determined by the slow phase. [8, 9]



Migraine-related vertigo or vestibular migraine

Migraine is a neurovascular disorder of the central nervous system that is caused by constriction and dilatation of intracranial blood vessels. The problem appears to be a dysfunction of ion channels in the aminergic nuclei of the brainstem and diencephalon. It is characterized by recurrent episodes of headaches, usually unilateral, and throbbing, with associated phonophobia, photophobia, and nausea. Headaches may occur with or without prodromal symptoms (aura). The aura consists of neurologic symptoms, mostly visual (such as scotomas-flashing or colored lights), photophobia, and/or paresthesias, likely a result of decreased local cerebral perfusion that passes across the cortex. Vestibular symptoms such as dizziness, vertigo, and tinnitus are less common but are increasingly being recognized. [10]

Migraine affects about 6-20% of men and 18-29% of women. [11, 12] Vertigo is 3 times more common in patients who suffer from migraine than controls. Therefore, establishing which patients have migrainous vertigo (MV) and which ones just have these conditions as separate entities is important. [13]

The relationship between vertigo and headache is variable. [14] Some patients experience the vertigo and headache as a completely separate event. In others, the headache can occur simultaneously with vertigo (25% of patients) or prior to the onset of vertigo (25% of patients). Vestibular symptoms precede headache in 50% of cases. Head motion intolerance is present in 30% of patients and typically persists after the acute attack of vertigo subsides. The duration of the vertigo can last from seconds (10%), minutes (30%), hours (30%) to days (30%). [14] Therefore, 10-30% of patients present with symptoms that are of typical duration of a migraine aura (5-60 minutes).

Most patients present with other migrainous symptoms that include photophobia, phonophobia, osmophobia, visual, or other auras. Photophobia is the most prevalent, present in 70%. These symptoms are extremely important to recognize because sometimes they are the only connection between the vertigo and migraine. Also, the patients should be asked about triggering factors such as food, hormonal changes (menstrual cycle), excessive stress, and sensory stimuli.

Hearing loss and tinnitus are not prominent symptoms. Hearing loss, when present, is usually mild and transient, without progression in the course of disease. Some patients can present with fluctuating hearing loss during the episodes, confusing the diagnosis with Meniere disease. Around 20% of patients report aural pressure for seconds to minutes at the beginning of the acute attack. [14]

Benign paroxysmal vertigo of childhood (BPVC) is considered to be an early manifestation of MV and a predictor for the development of migraine headaches. It is characterized by vertigo with nystagmus, nausea/vomit, and anxiety in an otherwise healthy child. Many of these children present with migraine later in life. [15]

A Korean study, by Lee et al, of children and adolescents who were patients in the otolaryngology departments of 11 hospitals, found that dizziness was most often caused by vestibular migraine and benign paroxysmal vertigo of childhood (BPVC) in children aged 7-12 years and that vestibular migraine was the most common cause in adolescents aged 13-18 years. In children aged 6 years or younger, vestibular migraine was the second most common cause of dizziness, after BPVC. [16]

A consensus about the diagnosis and treatment of migrainous vertigo is evolving. Like migraine itself, MV is diagnosed based on history and physical examination. Several authors proposed different criteria in retrospective studies. One proposed criteria defines definite MV and probable MV: [17]

  • Definite migrainous vertigo
    • Episodic vestibular symptoms of at least moderate severity (”moderate” is considered to interfere with daily activities)
    • Current or previous history of migraine per International Headache Society criteria
    • One of the following symptoms during 2 or more vertigo attacks: migrainous headache, photophobia, phonophobia, visual or other auras
    • Other causes of vertigo ruled out after appropriate investigation
  • Probable migrainous vertigo
    • Episodic vestibular symptoms of at least moderate severity (”moderate” is considered to interfere with daily activities)
    • One of the following: current or previous history of migraine per International Headache Society criteria; migrainous symptoms during a vestibular symptoms; migraine precipitants of vertigo in more than 50% of the attacks (food, sleep disturbances, hormonal changes); response to migraine medications in more than 50% of the attacks
    • Other causes of vertigo ruled out after appropriate investigation

Notice that the response to treatment is not considered a diagnostic criteria.

Basilar migraines are relative rare causes of migraines that involve pathology within the posterior circulation of the brain. Multiple neurologic symptoms including vertigo, dysarthria, dysphagia, and paresthesias precede the onset of the headache.

Examination of patients with a history of migrainous vertigo is typically normal. Spontaneous or positional nystagmus may be visualized during an acute attack. ENG testing may be normal or reflect a peripheral vestibular loss or central pathology. [8]

Treatment of headaches includes modification of lifestyle, elimination of trigger factors, treatment of acute attacks, and prophylactic medications, when indicated. Evidence-based guidelines for the management of migraine headaches have been published and are reviewed elsewhere. Prophylactic medications aim to reduce frequency of attacks and severity and may be indicated, depending on the number and severity of attacks, degree of disability, and response to acute attack treatments. The options include propranolol, valproate, amitriptyline, fluoxetine, gabapentin, and, more recently, topiramate. About 60% of patients have a reduction in symptoms.

Similarly to headaches, the vestibular symptoms of migrainous vertigo are managed with treatment of acute attacks and prophylaxis. [18] Acute attacks are managed initially with a vestibular suppressant. [19] The use of triptans for migraine-related vestibular symptoms is not well studied and may or may not benefit vertiginous attacks. Prophylactic treatment is indicated with frequent, severe, and disabling attacks. Beta-blockers, tricyclic antidepressants, and calcium-channel blockers are useful in preventing vestibular symptoms. Antiepileptic drugs such as valproate, gabapentin, and topiramate are effective and well tolerated. Changes in lifestyle and avoidance of trigger factors are important in preventing vestibular symptoms.

Vertebrobasilar disease

The vertebrobasilar system provides blood supply to the occipital, parietal and temporal lobes, thalamus, inner ear, cerebellum, and brainstem. The most common causes of vertebrobasilar disease (VBD) are embolism, large artery atherosclerotic disease, small (penetrating) artery disease, and arterial dissection. [20] Pathology within the vertebrobasilar system results in either recurrent episodes of transient neurologic deficits lasting minutes (vertebrobasilar insufficiency), TIA, or CVA.

A study by Paşaoǧlu found that among patients suspected of having central vertigo (without stroke) who were examined with computed tomography (CT) angiography, vertebral artery hypoplasia and stenosis of 50% or greater were seen more frequently than they were in the control group, with stenosis of 50% or greater found in 78 of 129 (60.5%) vertigo patients. [21]

Up to 25% of patients with VBD present with isolated vertigo. More frequently, VBD manifests with a combination of dizziness/vertigo, hearing loss, tinnitus, headache, nausea, visual disturbances, gait disturbances, paresthesias, motor weakness, and drop attacks. VBD symptoms are summarized into the “four Ds”: dizziness, diplopia, dysphasia, and drop attacks. Neurologic examination could be normal between attacks. Usually patients have risk factors for CVA and atherosclerosis, such as diabetes, hypertension, hyperlipidemia, hypercholesterolemia, hyperviscosity, and hypercoagulability.

Several specific syndromes are associated with ischemia to the territory supplied by anterior inferior cerebellar artery (AICA) or posterior inferior cerebellar artery (PICA). [22, 23] The territories vary among individuals; therefore, the clinical findings vary depending on the areas supplied by the ischemic vessel. Ischemia to the AICA distribution causes pontine syndrome. [23] The AICA supplies the lateral pons and gives off the internal auditory artery (IAA). Occlusion of this artery produces ischemia of the entire labyrinth and a degree of pontine ischemia, producing a syndrome that manifests as vertigo, tinnitus, and hearing loss. If the occlusion is distal, only the labyrinthine blood supply is compromised, producing symptoms and ENG findings that are identical to a peripheral disorder.

Ischemia to the PICA distribution causes Wallenberg syndrome (lateral medullary syndrome). [22] It is characterized with acute vertigo, nausea, and vomiting; ipsilateral facial pain and numbness; ipsilateral ataxia and decreased contralateral pain; and temperature sensation over the rest of the body; and ipsilateral Horner syndrome. Patients can also present with laryngeal and pharyngeal paralysis, leading to hoarseness and dysphagia.

In all patients in whom vertebrobasilar disease is suspected, imaging should be obtained. Imaging should include a magnetic resonance imaging (MRI) scan of the brain, as well as imaging of the vasculature with either an MR angiogram or a CT angiogram of the head and neck. A transcranial ultrasound that reveals flow in the vertebral arteries may also be helpful.

Treatment of VBD consists of treating the underlying pathology. Treatment is focused on controlling the risk factors for CVA and antiplatelet agents such as aspirin, dipyridamole, and pentoxifylline. [24] Chronic dizziness and disequilibrium usually improves with vestibular physical therapy. Treatment of TIA and stroke are beyond the scope of this review. [25]

Prognosis of ischemia to the posterior circulation differs significantly from anterior circulation. Acute basilar artery occlusion carries a very poor prognosis with a mortality rate higher than 80%. On the other hand, unlike the cerebral cortex, the brainstem is relatively resistant to ischemia, and recanalization therapy up to a period of 24 hours can still reverse the symptoms and sequelae.

Arnold-Chiari malformation

Arnold-Chiari Malformation consists of an abnormal displacement of the cerebellum and brainstem through the foramen magnum. The degree of displacement classifies the malformation in types I through IV. The most common is the type II, in which the cerebellar vermis, lower pons, and medulla is displaced. [26]

The associated symptoms are a result of the compression of the cerebellum and brainstem structures and stretching of cranial nerves. Patients can present with vertigo, ataxia, dysequilibrium, sensorineural hearing loss, headache, cranial nerve dysfunction (such as unilateral hypoglossal palsy), cervical pain, or weakness.

The diagnosis can be made by MRI, with the sagittal view being the most helpful in determining the degree of herniation. [27] The treatment is surgical. The results in terms of alleviating the vestibular symptoms are not well established, but case reports show some improvement.

Multiple sclerosis

Multiple sclerosis is an idiopathic demyelinating disorder of the central nervous system. It is thought to be an autoimmune disease, likely due to an autoantigen to one of the myelin proteins. The demyelinization occurs in different areas of central nervous system, most commonly in the white matter, with formation of plaques that disrupt signal conduction and lead to symptoms.

Typical onset is with optic neuritis, but in 5% of the cases vertigo is the presenting symptom. Over 50% of patients present with vertigo at one point in the course of the disease. The vertigo can last from hours to days. Nystagmus, when present, can be consistent with peripheral or central lesion. MS can mimic an VIIIth nerve lesion, when a plaque develops in the entry of the nerve root in the brainstem, producing vertigo, unilateral caloric weakness, and horizontal nystagmus. [28]

The diagnosis is made with imaging and CSF exam. On MRI, plaques can be seen in the white matter. On CSF, elevated levels of IgG can be identified. The treatment options are limited. Exacerbation episodes are treated with high-dose steroids and other immunosuppressants. [6]