It is important to remember vertigo is a symptom, not a diagnosis. Most of us have experienced some vertigo in our lives. However, this can be difficult for an individual to describe, so often, vertigo is described in various ways. One of the simplest forms of vertigo which many have experienced is the transient feeling of dizziness and perception of ourselves or the environment spinning around us after rapidly turning in circles. Often, nausea and vomiting will accompany these symptoms.
The etiology of vertigo is typically due to a disturbance of the vestibular system, semicircular canals, or cranial nerve 8. This disturbance could be related to damage of one of these organs or simply confused neuronal input. It is important to remember that the central nervous system receives inputs bilaterally from these structures/systems, assembles the input and then, forms a response. The central nervous system (CNS) also coordinates these bilateral inputs with our visual and sensory inputs creating an overall picture of whether we are moving in space/time or if the environment around us is moving. Suffice it to say that conflicting inputs from these various symptoms overwhelm the central nervous system causing “dizziness,” nausea, and the perception of movement.
The following are the various causes of vertigo:
Benign paroxysmal positional vertigo (BPPV), Meniere's disease, vestibular neuritis, labyrinthitis, herpes zoster, acoustic neuroma, otitis media, perilymphatic fistula, aminoglycoside toxicity, viral infections, and Cogan syndrome.
Brainstem ischemia/infarction, vertebrobasilar insufficiency, space-occupying lesions, demyelination syndromes, vestibular migraine, and Chiari malformation.
Benign Paroxysmal Positional Vertigo
Benign paroxysmal positional vertigo is classically described as a sudden onset of spinning brought on by a rapid head movement or a quick turn in bed before getting up. There is no associated ear pain, tinnitus or hearing loss. The pathophysiology behind this is usually displacement of otolith or calcium debris located in the posterior semicircle canal. This type of vertigo classically can be made worse with the Dix Hallpike maneuver and subsequently fixed with the Epley maneuver by relocating these otoliths. Other less commonly used maneuvers include Semont, Lempert, and Hamid.
Peripheral Vertigo Causes
Approximately 80% of vertigo is peripheral whereas approximate 20% is central in origin. Of this 80%, benign paroxysmal positional vertigo (BPPV) is by far the most common cause of peripheral vertigo.
A disturbance of the vestibular system, semicircular canals, or cranial nerve 8 is the underlying issue. This disturbance could be related to damage of one of these organs or simply confused neuronal input. It is important to remember that the central nervous system receives inputs bilaterally from these structures/systems, assembles the input and then, forms a response. The CNS also coordinates these bilateral inputs with our visual and sensory inputs creating an overall picture of whether we are moving in space/time or if the environment around us is moving. Suffice it to say that conflicting inputs from these various symptoms overwhelm the central nervous system causing dizziness, nausea, and the perception of movement.
Vertigo is broken down into two types: peripheral and central. As the main focus of this chapter is on peripheral vertigo, we will only touch slightly on central vertigo to help distinguish between the two.
Usually, peripheral vertigo is, although not always, due to a benign process whereas central vertigo often indicates a more serious pathology.
Peripheral vertigo is described as dizziness or a spinning sensation. Other symptoms associated with peripheral vertigo include:
The diagnosis and workup consist of taking a very accurate and detailed history along with symptomatic/physical findings. Peripheral vertigo is typically episodic and acute/severe. Alternatively, central vertigo typically is over a longer duration of time and “most” of the time, less severe symptoms occur. Peripheral vertigo usually can be made worse with head movements and typically has been associated with horizontal/rotary nystagmus which is fatigable and unidirectional.
Central vertigo can have nystagmus in any direction is not fatigable and typically multi-directional.
The Dix Hallpike test can be used to aid in the diagnosis of peripheral vertigo typically making symptoms worse and nystagmus more obvious.
Other specialized tests include:
Treatment usually involves giving the body time to heal and treatment of the underlying process. There is some data to suggest, antihistamines, benzodiazepines, corticosteroids, antiemetics, and anticholinergic’s may be of use depending on the etiology of peripheral vertigo. Vestibular rehabilitation therapy (VRT) may also offer relief to some patients. Vestibular rehabilitation therapy is a form of physical therapy which takes advantage of the plasticity of the brain using specialized exercises and head movements to help gaze and gait stabilization.
The differential diagnosis of peripheral vertigo can be vast and will not be discussed in depth here however it is important to always consider stroke, infection and other potentially treatable etiologies.
The prognosis for peripheral vertigo is typically quite favorable. It may lead to some morbidity however once the etiology is correctly identified symptoms can usually be quite tolerable if not completely resolved.
The management of peripheral vertigo is best done with a multidisciplinary team including nurses and pharmacists. Many treatments exist for peripheral vertigo but none is reliably effective. In many cases, a trial of one agent is performed and if it does not work, another remedy is tried. The quality of life of most patients with peripheral vertigo is poor. Drugs like antihistamines are often not well tolerated and corticosteroids have serious adverse effects.
|||Wang X,Strobl R,Holle R,Seidl H,Peters A,Grill E, Vertigo and dizziness cause considerable more health care resource use and costs: results from the KORA FF4 study. Journal of neurology. 2019 May 22; [PubMed PMID: 31119449]|
|||Jahn K,Lopez C,Zwergal A,Zur O,Cakrt O,Kellerer S,Kerkeni H,Tjernström F,Meldrum D, Vestibular rehabilitation therapy in Europe: chances and challenges. Journal of neurology. 2019 May 17; [PubMed PMID: 31102020]|
|||Rivera M,Porras-Segovia A,Rovira P,Molina E,Gutiérrez B,Cervilla J, Associations of major depressive disorder with chronic physical conditions, obesity and medication use: Results from the PISMA-ep study. European psychiatry : the journal of the Association of European Psychiatrists. 2019 May 14; [PubMed PMID: 31100609]|
|||Mathkour M,Helbig B,McCormack E,Amenta PS, Acute Presentation of Vestibular Schwannoma Secondary to Intratumoral Hemorrhage: A Case Report and Literature Review. World neurosurgery. 2019 May 16; [PubMed PMID: 31103763]|
|||Becares-Martinez C,Lopez-Llames A,Arroyo-Domingo MM,Marco-Algarra J,Morales Suarez-Varela MM, [What do MRI and CT scan provide us in patients with vertigo and dizziness? A cost-utility analysis]. Revista de neurologia. 2019 Apr 16; [PubMed PMID: 30963529]|
|||Huppert D,Straube A,Albers L,von Kries R,Obermeier V, Risk of traffic accidents after onset of vestibular disease assessed with a surrogate marker. Journal of neurology. 2019 Apr 9; [PubMed PMID: 30963255]|