Dizziness is a common complaint that presents non-specifically in many clinical scenarios. It is a complaint that features in arrhythmias, hypotension, shock states, reflex mediated syncope or presyncope, vertigo, and most critically cerebellar infarctions. While we may not always be able to determine the primary cause of dizziness, we do have clues that can assist us in the right direction; namely, testing for central causes vs peripheral causes.
Vertigo is a term that refers to the sensation of motion or spinning while the body is at rest. This is commonly described as the sensation that the room is “moving around me even though I am sitting still”. It may occur when lying flat or upon rising to a sitting or standing position, and is often accompanied by nausea, and ataxia. As we know, there are two areas that are primarily responsible for interpreting the position of the body in space: the inner ear, and the cerebellum.
Peripheral vertigo refers to a cause arising within the inner ear, either unilaterally or bilaterally. This may involve lesions of the labyrinths or the vestibular nerves themselves. A common cause is Benign Paroxysmal vertigo, which refers to intermittent episodes that resolve on their own and then recur spontaneously again. BPV is caused by free floating otoconia, which are calcium carbonate crystals, that have dislodged from their normal location in the inner ear and have moved into one or both of the labyrinths. When the head is moved, these otoconia shift inside the labyrinth, causing a false sense of motion. It typically is alleviated by lying still, and exacerbated by changes in position. When the head is moved, the patient will exhibit vertical torsional nystagmus that beats toward the affected affected ear. Other potential causes of peripheral vertigo include Acute prolonged vertigo, and Meniere's Disease. Both of which require testing we cannot do in the pre-hospital setting.
Central Vertigo refers to causes originating in the cerebellum, in the brainstem. In general, the initial presentation of these patients will be similar to that of peripheral vertigo with a couple important exceptions that we can use to figure things out. Patients with peripheral vertigo will be “dizzy” but generally tolerate ambulation with assistance. However, those with central causes will not be able to tolerate walking, as the ataxia will be very pronounced. Nystagmus is another key indicator here. What we are testing for here is GAZE NYSTAGMUS. In patients with peripheral causes of vertigo, nystagmus will be present with movement of the head, but it should resolve when the patient fixes their eyes on a specific point, such as your finger or a pen light. In central vertigo, the nystagmus will not resolve with fixed gaze testing. For this reason, the visual fields test is important to help look for possible cerebellar involvement. In addition to visual testing, patients with cerebellar infarctions may present with other signs of posterior stroke, such as:
Ataxia
Dysarthria
Headache
Nausea
Vomiting
If the infarction is hemorrhagic in nature, we may also gradually see signs of elevated intracranial pressure (Cushing's Triad), and alterations in level of awareness.
In general, every patient who presents with a chief complaint of “dizziness” needs a full assessment that includes:
Vitals
12-lead
BGL
Stroke exam
Pupils and visual field testing
Orthostatic testing to look for provoking and palliating factors.
A good rule of thumb is to assume it is a stroke until you can rule out other causes. That being said, vertigo is not featured in many stroke bypass protocols, so we need to be thorough in ensuring other red flags are not present.
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