Dizziness explained, part 1: how it arises

In the first of a two-part series, Toby Commerford gets down to the nitty-gritty of dizziness. Part 2 will be published in a fortnight.

DIZZINESS is a by-product of the fact that we have four distinct senses or signals continuously flooding our central nervous systems (CNS) regarding bodily movement. Normally, these marry up and are congruent – which causes no trouble. However, if disease targets one of these “we-seem-to-be-moving” senses, such that it ends up sending incorrect and erroneous body–motion signals to the CNS, a mismatch occurs. This incongruity triggers dizziness — this is often combined with other unsettling vestibular symptoms to form a “vestibular syndrome”.

Given that dizziness can be a vexed topic, this is the first of two plain-English articles aiming to make “dizziness” comprehensible; my own interest in disseminating these basic ideas stemmed from a growing awareness of my ignorance on the subject. This article will set the scene with the basics on how dizziness arises mechanistically. In the second instalment, this information will be coupled with an overview of a new way in which “dizziness” cases can be approached at the bedside – differing from a former well known paradigm on how to assess the dizzy patient, one replete with issues.

Back to basics

The idea that we have “five senses” is not strictly true. Not only is the “smell, sight, taste, touch and sound” maxim reductionist – considering, for example, that we also have abundant visceral senses collectively known as “interoception” – but it also fails to acknowledge a variety of senses of “movement” or “motion”. The perception of “self versus world motion” is built up within the CNS from various cues – as mentioned, there are four of these, and they feed ever-changing “motion information” into the CNS constantly. They are as follows:

• Head (ie, skull) movements of all types are sensed directly by a bilaterally-arranged pair of “head motion sensors” in the labyrinth of the right and left inner ears. Effectively, we possess specialised proprioceptors just for the head. Movement types sensed by these organs include tilting or falling “like a telegraph pole” (so-called “linear acceleration”; think of “otoliths, the saccule and utricle”; spinning or rotating (so-called angular acceleration; think of semicircular canals); or travelling along a desired pathway (eg, going up in a lift, or driving; so-called “translation”). The term “vestibular” refers to the sensing of motion of the human head specifically (and as opposed to other parts of the body); as described later, however, the term “vestibular system” is operationally defined more broadly and clinically. Notwithstanding, whichever type of head motion is being detected by the right and left vestibular organs, the system still functions in the same overarching manner. The right and left vestibular organs feed into the brainstem bilaterally via the vestibulocochlear (8th) nerves, and the CNS concludes that the head is moving when there is a difference between the two sides. The 8th nerves fire continually (ie, “tonically”). As a rule, if both sides fire at the same frequency (eg, both at 125 Hz), the net difference of zero is interpreted as “the head is stationary”. In contrast, differences in firing frequencies are taken to mean that the head is “on the move” (whether tilting, rotating or translating). Precisely because the system is bilateral and firing tonically, any unilateral (hemi-) lesion along the three-neuron vestibular pathway may be misinterpreted as “our head is moving”, even if nothing else says so, triggering the onset of dizziness.

This is a schematic view of anatomical basics pertaining to dizziness (please note that the vermis is a unitary structure in vivo) (Figure 1):

Figure 1. Coronal brainstem view

Shown below (Figure 2) is the way modern studies of pathway-anatomy suggest the vestibular sense distributes itself – that is, how any “head is moving” signals (in red) reach the brainstem, thalami and cortices after deriving from the labyrinths bilaterally. It forms a sort of  “rope ladder”.

Figure 2. Vestibular sense distribution

• Next, we have visual input, specifically motion of things we can see. There are unique cells in the retina and beyond, which only fire when something external moves in front of us. As such, we have a specific sensory system for visual motion or “optic flow”.
• Next, we have peripheral body and limb senses, most pertinently “proprioception” – which is the fascinating dynamic sense of body motion and position imaginable even with the eyes closed, conveyed to the brain via the dorsal column/medial lemniscus pathways. Mechanoreception from the feet is also relevant in conveying bodily movement.
• Finally, and more cryptically, self-motion can be suggested by our own brains, because to move we need internal motor commands. Accordingly, if we divert a copy of our own voluntary commands to move (like a “cc’d” email), it adds further weight to the “we are moving” percept building up, which is sometimes called an “efference copy”.

This all said, what is actually done with the cues regarding bodily motion? It is likely that all four converge onto neurons downstream in the CNS in various combinations – some receiving head- and visual-motion signals concurrently, others with different multimodal inputs – collectively described as “multisensory” cells. It is likely that these neurons connect to each other in a network (Figure 3), though this is not well understood. Individual motion-sensing modalities may be imperfect: for example, head-motion signals can be ambiguous because otoliths fire both when we tilt from standing (eg, falling like a telegraph pole) and move along by ‘translation’ (eg, driving). Similarly, because the world moves when we move, when visual motion is detected, the CNS needs to ‘decide’ if the movement is internal (us) or external (environmental). Consequently, we need multisensory neurons to accurately compute or ‘decide’ the exact reality of how we are moving (by analysing several motion-cues concurrently).

Figure 3. Schematic diagram of multisensory cells (possibly networked together) and how they may link with downstream processes after conclusive computational analysis of our bodily movements

What is the actual purpose of detecting bodily motion in the first place?

One key reason for detecting bodily movements is that self-motion blurs vision; accordingly, we need ocular motor systems to maintain clear vision as we move. Another key purpose is the detection of falling from an upright stance – such that we produce counteracting “righting reflexes”. Another is so that we can navigate through the environment (knowing where you are, topographic orientation, partially depends on awareness that you have moved). Further to this, input suggesting bodily motion feeds into the cortex both at a perceptual level (where a conscious awareness and emotional feeling is engendered about the movement), and at a “vegetative” level, where it may trigger autonomic responses (such as vomiting or tachycardia).

Accordingly, it is likely that clusters or networks of multisensory cells are stationed throughout the CNS, connecting with (and influencing) core regions involved in maintaining visual stabilisation, balance, and conscious perceptions of verticality and self-motion.

Definitions of the term “vestibular”, related symptoms and “vestibular syndromes”

Although the word vestibular technically denotes the sensing of head-motion – given labyrinthine physiology – the phrase vestibular system is often defined more broadly as a collective term for the many neural processes involved in visual stabilization and balance when faced with bodily movement. In clinical practice, the vestibular system denotes the pathways and networks through which disease leads to pathological dizziness, unsteadiness and visual blurring.

Accordingly, as doctors, although “I’m dizzy” may be the presenting complaint we hear, there are actually many so-called vestibular symptoms related to pathology of visual stabilization, balance, verticality, and self-motion consciousness. These are documented in the early work of the International Classification of Vestibular Diseases. These symptoms (eg vertigo, unsteadiness, visual tilting) commonly co-exist, and emerge together in particular time-frames and patterns, known as vestibular syndromes (a focus of the next instalment). It is, incidentally, worth noting that many patients experiencing a vestibular syndrome are worsened by head motion; if head motion exacerbates the dizziness, this is not diagnostic in any particular way. Further in relation to poor visual stabilisation, it is worth noting that there are two major causes of jerk nystagmus – either a focal vestibular lesion, such that the eyes (+/- the neck) move because they receive erroneous signals suggesting the head is moving when it is actually stationary, or damage to the aforementioned neural integrator (ie, gaze-evoked nystagmus). Nystagmus may cause unpleasant visual blur, which patients may describe as vertigo – and which the ICVD denote as external vertigo.

The basics on how certain pathologies can cause the unleashing of dizziness

Given that vestibular syndromes occur when a network of neurons is activated across a wide expanse of the brain, diseases or drugs causing dizziness can be either focal (eg, positioned unilaterally along a vestibular pathway) or global (eg, transient hypoperfusion of the brain due to hypotension). The pathogenesis underlying symptoms may be incompletely understood, but as we are ultimately dealing with CNS neurons, diseases are likely either localised or diffuse.

In terms of focal lesion types, these may include:

• New unilateral vestibulopathies. Acute or transient lesions along one of the pathways signaling head motion (in red, Figure 2) may grossly reduce (or pathologically increase) the firing rate of the afflicted side. If the right-sided pathway – whether in the periphery (labyrinth and 8th nerve) or centrally (brainstem, thalamus etc) – are damaged, its firing rate drops to 0 Hz, while the intact left side continues to fire at 30-100 Hz. The disparity leads to dizziness because the head is actually still, but the vestibular signal traversing into upstream multisensory cell clusters suggests otherwise.
• Bilateral vestibulopathy. In this state, patients have oscillopsia or movement-induced blur on walking (because the vestibulo-ocular reflex loses all input), but patients tend not to have any explosive dizziness at rest (because both 8th nerves stop firing, and so they are not asymmetric).
• Vestibulocerebellar disease. This may cause movement-induced visual blurring (eg, if the flocculus fails to tune the VOR), truncal sway (if the vermis is damaged), and it may cause gaze-evoked nystagmus. As much as the flocculus helps maintain lateral gaze against elastic recoil forces on the eyes, it also helps maintain the eyes in their primary straight ahead position. There is a tendency for the eyeballs to drift up over time – consequently, the healthy flocculus sends continuous signals inhibiting this drift, whilst the medulla sends complementary signals promoting downward-turning of the eyes. Damage to these sites causes vertical nystagmus (downbeat and upbeat, respectively), which patients may also describe as dizziness.

Dr Toby Commerford is a consultant geriatrician at Royal Adelaide Hospital, is course coordinator for geriatrics at the University of Adelaide’s Rural School, and practices remote and rural outreaches to Port Augusta and Murray Mallee. He is also the lead singer in a rock band.

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