eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Vertigo & Dizziness

CNS Causes of Vertigo

Author: Carol A Bauer, MD, Associate Professor, Department of Surgery, Division of Otolaryngology, Southern Illinois University School of Medicine
Contributor Information and Disclosures

Updated: Apr 30, 2007

Introduction

Background

The symptom of vertigo is nonspecific. Vertigo occurs when an imbalance or disturbance in vestibular function exists anywhere in the peripheral or central vestibular system (ie, labyrinth, vestibular nerve, brain stem, cerebellum, cortex). The etiology of vertigo includes familial, infectious, neoplastic, metabolic, toxic, vascular, autoimmune, and traumatic causes. Distinguishing the site and cause of the lesion that results in vertigo is important because some causes of central vertigo can be life threatening and require immediate attention.

Pathophysiology

The sensation of balance is the result of appropriate information detected by the vestibular, ocular, and proprioceptive sensory receptors that is then properly integrated within the cerebellum and brain stem. Proper gait, posture, and visual focus during head movement all depend on an intact sense of balance. Loss of sensory information, central integration, and output control mechanisms all result in a sense of imbalance.

Central causes of vertigo result from either a disruption of central integrators (ie, brain stem, cerebellum) or a sensory information mismatch (ie, from the cortex). Lesions that affect the vestibular nerve or root entry zone (ie, cerebellopontine angle [CPA] lesions) result in imbalance by affecting primary vestibular sensory information.

Race

No racial predilection exists for CNS causes of vertigo.

Sex

Men and women are affected differently by different causes of CNS vertigo. Vestibular migraine, for example, shows a predilection for women.

Age

CNS causes of vertigo typically affect older population groups because of the associated risk factors of vascular causes of vertigo, such as hypertension, atherosclerosis, and diabetes mellitus.

• Younger population groups are more commonly affected by migraine headaches and multiple sclerosis (MS).
• Cerebellar tumors affect a bimodal population of children and adults.
• CPA tumors typically affect people in the fifth to eighth decades of life.

Clinical

History

• CNS causes of vertigo can manifest in various ways. Vertigo can be acute and severe and last for days, or it may be recurrent, with attacks that last for minutes to hours. Less often, central vertigo appears as brief episodes of vertigo brought on by changes in head or body position. CNS disease can manifest as chronic or episodic gait ataxia without associated vertigo.
• Patients may describe an intense or severe sensation of movement, tilting, or imbalance; the sensation is aggravated by movement and improved by remaining stationary. Discriminating between vertigo (the sensation of movement or spinning) and lightheadedness is important. Lightheadedness is often a symptom of a metabolic or cardiovascular abnormality. The causes of presyncopal dizziness include hyperventilation, orthostatic hypotension, and decreased cardiac output.
• The cause of vertigo is often revealed by the patient's history and physical examination.
• • In migraine-associated vertigo, the patient reports a history of acute-onset vertigo that lasts minutes to a few hours or many hours to days. Vertigo may precede, follow, or appear simultaneously with the headache (migraine without aura), and vestibular symptoms range from mild to severe. Vertigo may occur with the additional symptom of aura (ie, visual and somatosensory paresthesias) before a headache (ie, migraine with aura). Less commonly, vertigo is a symptom of basilar migraine, which is suspected when the vertigo is accompanied by binocular visual deficits, diplopia, dysarthria, hearing loss, ataxia, or decreased consciousness.
  • Several mechanisms can cause vertigo and dizziness in persons with cerebrovascular disease. Presyncopal lightheadedness occurs with diffuse cerebral ischemia from any etiology (eg, orthostatic hypotension, myocardial infarction). Postural imbalance or disequilibrium results from loss of any component of the balance pathway (ie, vestibular, somatosensory, central integration, motor output) caused by transient ischemia or infarction. Vertigo can occur with cerebrovascular disease that involves the vertebrobasilar circulation, which supplies the labyrinth, the lateral pontomedullary region that contains the vestibular nuclei, and the cerebellum.
  • In vertebrobasilar artery (VBA) insufficiency, vertigo is sudden in onset, lasts only minutes, is associated with nausea and vomiting, and is usually accompanied by a range of neurologic deficits (eg, extremity weakness, numbness, incoordination, and dysarthria; diplopia; field defects; tinnitus; hearing loss; loss of consciousness; drop attacks). Isolated vertigo without additional symptoms can be the presenting manifestation of vertebrobasilar ischemia.
  • A subgroup of patients with episodic, spontaneous, or positional vertigo experience poor autonomic regulation. These patients usually have a low ( <100 mm Hg) systolic blood pressure and associated symptoms of palpitations, chronic fatigue, sleeping disorders, cold extremities, and fainting spells. They also usually have a history of mitral valve prolapse.
  • Symptoms and signs of posterior fossa cerebrovascular disease include vertigo, tinnitus, and ataxia. Symptoms may be transient, permanent, recurrent, or isolated. Stroke syndromes that involve the posterior circulation vary depending on the involved territory. Wallenberg syndrome (ie, lateral medullary syndrome) appears with vertigo, nausea, vomiting, imbalance, ipsilateral facial numbness and weakness, diplopia, dysphagia, and dysphonia. Infarction of the dorsolateral pontomedullary region results in labyrinthine injury (ie, severe vertigo, nausea, vomiting, hearing loss) in addition to the signs and symptoms of Wallenberg syndrome.
  • Cerebellar infarction also occurs with severe vertigo, nausea, vomiting, and ataxia. When cerebellar infarction occurs without any other associated neurologic or audiologic symptoms, the presentation may be attributed to viral neuronitis (VN). Such cases of pseudo-VN usually occur after infarction of the nodulus and uvula, territory supplied by the medial branch of the posterior inferior cerebellar artery (mPICA). Cerebellar signs that affect the extremities can be minimal or absent in mPICA infarction of the vestibulocerebellum. Infarction of the territory supplied by the anterior inferior cerebellar artery (AICA) rarely presents as pseudo-VN, since cochlear ischemia manifested as hearing loss and additional brainstem signs, such as facial palsy, are typically present.
  • Basilar artery syndrome results from infarction of the pons. Symptoms include vertigo, hearing loss, ataxia, ophthalmoplegia, blindness, and regional sensory losses.
  • Chiari malformation is a structural abnormality of the posterior fossa and craniocervical junction. A range of hindbrain deformities, from cerebellar tonsil to brainstem herniation through the foramen magnum, is associated with the defect. Neurotologic symptoms may result from conditions that range from stretching of the lower cranial nerves to brainstem distortion to altered cerebrospinal fluid dynamics. Subjective reports of vertigo and imbalance have been reported in 70% of patients with Chiari 1 malformations.
  • Patients with cerebellar tumors may present with positional vertigo, imbalance while walking and standing, and headaches. Specific features depend on tumor location (eg, lateral, medial, ventricular), tumor size, and growth rate. Primary cerebellar tumors typically occur in children. In adults, a cerebellar tumor usually results from metastasis.
  • Patients with temporal lobe tumors may present with recurrent attacks of vertigo that last minutes. This vertigo may be followed by transient disorientation, amnesia, and dysphasia.
  • Patients with brainstem lesions (ie, neoplastic, vascular, posttraumatic) may have vertigo as a presenting symptom. The vertigo may be brief or prolonged, depending on the extent of damage to the brainstem structures.
  • Cerebellopontine angle (CPA) tumors typically result in disequilibrium or unsteadiness rather than a sensation of vertigo. However, sudden change in tumor size with hemorrhage or disruption of regional blood flow to the labyrinth may precipitate vertigo. Tumors in the CPA are most likely to be vestibular schwannomas, followed by meningiomas, lipomas, cholesteatomas, and metastatic tumors.
  • Vertigo is the initial presenting symptom in 5% of cases of MS and is experienced by 50% of patients during the course of their disease. The vertigo may last several days to weeks; it may be positional in nature and is often associated with diplopia and facial numbness and weakness. Disseminated encephalomyelitis may also manifest with isolated recurrent episodes of vertigo and must be distinguished from MS.
  • Posttraumatic vertigo may be peripheral in origin (eg, benign paroxysmal positional vertigo, perilymphatic fistula, labyrinthine concussion, labyrinthine fracture) or central (eg, cerebral concussion). Postconcussion syndrome usually follows a mild head injury. Symptoms are characterized by vertigo, headaches, blurred vision, diplopia, fatigue, and personality changes.
  • Familial periodic ataxia syndromes represent a rare form of chronic recurring bouts of episodic vertigo. Patients have a family history of recurrent spells of vertigo. Presenting signs and symptoms include recurrent vertigo, prominent nausea and vomiting, diplopia and dysarthria with the spells, and a progressive truncal ataxia. Spells are precipitated by physical exertion or emotional stress.
  • CNS infection rarely causes vertigo. Patients with Lyme neuroborreliosis may have vertigo as a presenting feature of Lyme disease encephalopathy. Inflammatory, postinfectious disseminated encephalomyelitis can occur after various bacterial or viral infections, and vertigo may be a presenting symptom of the central disease.
  • Superficial siderosis of the CNS manifests with bilateral hearing loss and gait ataxia. Recurrent episodes of positional vertigo can also result from this rare disease. Subarachnoid hemorrhage secondary to distant trauma, cerebral or cerebellar tumors, and vascular disease results in hemosiderin deposition and subsequent dysfunction.
  • Psychogenic vertigo is a manifestation of panic or anxiety disorder. Patients describe a sensation of unsteadiness, vertigo, lightheadedness, and, less often, nausea and vomiting with the symptoms.

Physical

• During asymptomatic periods, patients with migraine-associated vertigo have normal physical examination findings. During a migraine, patients may have motion intolerance, diaphoresis, and vomiting but rarely experience dysarthria, aphasia, hemiparesis, or extremity ataxia. Occasionally, nystagmus is observed during an attack.
• When patients are symptomatic, a cardiac examination may reveal arrhythmia as the cause of symptoms. If hyperventilation is suspected, having the patient hyperventilate may precipitate the symptoms. Orthostatic changes in pulse and blood pressure should be documented if accompanied by symptoms of lightheadedness.
• Direction changing, gaze-evoked nystagmus, and severe truncal ataxia with limb incoordination are findings associated with cerebellar infarction. Lateral medullary infarction also causes direction-changing nystagmus; however, patients have associated signs that indicate brainstem damage, including decreased gag reflex, facial numbness, Horner syndrome, and dysphonia. Saccadic eye movements are disrupted, and the patient's gait is ataxic. Lateral pontomedullary syndrome also appears with nystagmus, defective saccades, and hearing loss.
• CPA tumors that cause vertigo also cause unilateral hearing loss and may occur with nystagmus. Nystagmus may be evident only in the dark or with Frenzel glasses, which remove visual fixation. A head thrust test may reveal unilateral vestibular weakness. Large tumors may cause subtle facial weakness, decreased corneal reflex, and facial dysesthesia.
• Differentiation between central and peripheral causes of vertigo is facilitated by a precise oculomotor examination. Spontaneous nystagmus that cannot be suppressed with visual fixation; nystagmus that changes direction with gaze; purely vertical, horizontal, or torsional nystagmus; and saccade dysmetria (overshoot and undershoot) are all signs that a potential central abnormality is the cause of the vertigo. Pseudo-VN can be reliably differentiated from true VN by using the head thrust test and caloric testing. Patients with pseudo-VN have a normal head thrust test result and normal caloric responses on electronystagmography (ENG).
• Positional or positioning vertigo of central origin usually presents with additional signs of oculomotor dysfunction, including disrupted saccadic pursuit and gaze-evoked nystagmus.
• Paroxysmal positional nystagmus of central origin usually does not decrease with repeated positioning maneuvers, has no latency of onset, lasts longer than 60 seconds, is often vertical in direction, and may change direction with different head positions. Positioning or positional nystagmus that is not associated with a sensation of vertigo represents a central lesion. Paroxysmal nystagmus with vertigo of peripheral origin, usually due to canalithiasis or benign paroxysmal positional vertigo (BPPV), can be differentiated from central paroxysmal nystagmus based on the direction of the eye movements. Nystagmus due to BPPV is always a combination of vertical and torsional eye motion. Paroxysmal nystagmus that is unidirectional (downbeat, upbeat, torsional) results from central lesions. The exception is nystagmus from canalithiasis that affects the horizontal canals. This nystagmus is either geotropic or ageotropic and, therefore, cannot be distinguished from a central lesion.
• Vertigo associated with panic attacks can sometimes be elicited by having the patient hyperventilate. Most patients with psychogenic vertigo do not have any pathologic findings on otologic or neurologic examination.
• The head thrust test is a useful bedside maneuver for determining the site of a lesion that results in vertigo. In this test, the horizontal vestibuloocular reflex (VOR) is assessed by the examiner, who applies brief, small-amplitude, rapid turns of the patient's head across the midline, first to one side and then the other. The patient is instructed to maintain visual focus on the examiner's nose during each head thrust. The examiner observes for corrective saccades at the conclusion of each head thrust, indicating a deficit in the horizontal VOR in maintaining gaze stability.

Causes

• Central vertigo syndromes that result from acute vascular events most commonly result from a combination of hypertension and regional atherosclerosis.
• Less commonly, arterial dissection secondary to neck extension, rotational injury, or osteoarthritic spurs is the cause of disturbed posterior fossa blood flow.
• Migraine headaches and presyncopal lightheadedness are 2 forms of regional and global ischemia that may appear with vertigo or imbalance as the primary symptom.
• Pathological spontaneous and positional nystagmus is observed in most patients during an attack of acute vestibular migraine. The direction of the nystagmus depends on the location of central dysfunction and may include torsional, downbeat, and upbeat nystagmus. Hearing loss is typically not observed during a migraine vertigo attack, although aural fullness and pressure have been reported.

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