Neuroscience Clerkship at UH/VA
 

CENTRAL VS. PERIPHERAL VERTIGO

 

Vertigo refers to the subjective feeling of movement of self or the environment in the absence of true movement. Vertigo is a frequent symptom that results from a variety of etiologies, some benign and others serious. One of the more important differentiating features is determining if the vertigo has a peripheral or central etiology. Making this distinction is very important as the causes, and thus clinical management of peripheral versus central vertigo, can vary significantly.

Peripheral vertigo generally refers to vertigo which arises from dysfunction of the vestibular apparatus in the inner ear (figure below) or its connecting vestibular nerve (CN VIII). In addition to hearing, the inner contains the bony labryinth where the semicircular canals and utricle/saccule are located. These structures sense linear and angular motion, and are essential in the maintenance of balance and various vestibular reflexes.


Central vertigo results from dysfunction of the central connections of the vestibular apparatus including the vestibular nuclei in the brainstem and their connections, especially to the cerebellum. The vestibular nerve (CN VIII) is usually considered part of the peripheral vestibular system (essentially being a peripheral nerve). However, in the case of an acoustic neuroma of CN VIII, if the neuroma is large, it can compress the cerebellopontine angle and result in central vertigo as well.

The diagram below summarizes some of these pathways (you do not need to memorize these for the exam).


DIFFERENTIAL DIAGNOSIS OF VERTIGO

Peripheral Central
Benign Paroxysmal Positional Vertigo (BPPV) Vertebrobasilar ischemic stroke (cerebellar, brainstem)
Labyrinthitis (viral or post-infectious) Vertebrobasilar hemorrhagic stroke (cerebellar, brainstem)
Meniere’s disease Demyelinating (multiple sclerosis)
  Tumor – of the cerebellar-pontine angle, brainstem or cerebellum.
CN VIII tumor Migraine (vertebrobasilar)
Perilymphatic fistula Partial seizure
  Infection (abscess)
  Neurodegenerative disease involving brainstem and/or cerebellum
Drug-induced (e.g., aminoglycosides) Drug induced (e.g., anticonvulsants)
 

 

The diagram above illustrates the Dix-Hallpike maneuver (also known as the Barany maneuver), a provocative test to try to reproduce the patient’s vertigo. The findings can be helpful in differentiating a peripheral from central cause of vertigo. (A) The patient begins in the sitting up position. The examiner turns the patient’s head 45 degrees from the midline. (B) Next, with the head kept 45 degrees from the midline on either side, the patient is leaned back with head tilted back and one ear directed to the ground. The patient keeps eyes open during the test. The examiner checks for the following:

Latency of nystagmus (time to onset of nystagmus)

Duration of nystagmus

Direction of fast phase of nystagmus

Reproducibility of the patient’s symptoms/signs (e.g., nausea, vomiting, vertigo, nystagmus)

Fatiguability of the response (lessening of provocative response with repetition of the maneuver)


The table below summarizes the findings from the patient's history, examination and/or provocative maneuvers that help differentiate peripheral versus central pathology.

CLINICAL DIFFERENTIATION OF PERIPHERAL VERSUS CENTRAL VERTIGO

Symptom / Sign Peripheral Central
Latency of nystagmus with head movement Usually a latency; range 0-40 sec (mean 7.8) No latency; begins immediately
Duration of symptoms < 1 minute Symptoms may persist
Fatigability (lessening signs and symptoms with repetition of provocative maneuver Yes No
Nystagmus appearance and direction Fixed direction, usually torsional and horizontal Changing direction, often pure vertical, horizontal or torsional
Intensity of symptoms Severe vertigo, marked nystagmus, nausea, vomiting Usually mild vertigo, less nystagmus, rare nausea
Reproducibility Inconsistent Consistent
Fixation (eyes open, fixating on a distant object) Improves symptoms Little effect
Hearing loss and/or tinnitus Common Uncommon
Other brainstem signs (e.g., diplopia, facial numbness, dysarthria, etc.) Absent May be present

Adopted from Bradley, Daroff et. al, Neurology in Clinical Practice, 4th Edition.