This essay is by Jim Meadows, BScPT, MCPA, FCAMPT. It is the third in a series on clinical assessment of vertebrobasilar insufficiency.
In the first essay, VBI: the 5 Ds, I argued that using the 5 Ds as a group identifier of the presence of vertebrobasilar ischemia was useless and in fact dangerous. I argued from available evidence that most of the symptoms were not commonly associated with traumatic VBI, and that the second most common symptom — headache — was not included in the 5 Ds because it had the misfortune to start with “H.” The exceptions were dizziness and dysarthria, one of which we will discuss in this essay.
My second argument was that most commonly there were no clear neurological symptoms at the onset of VB stroke, let alone the transient syndrome that would likely occur with our patients. For these reasons the 5 Ds — as a group or individually — are neither useful as a screening protocol nor as a diagnostic tool. They are neither sensitive (unless dizziness as a single symptom is used, in which case it is too sensitive) nor specific for VBI.
This essay will look at the most common symptom of VBI — dizziness — and how to begin to appreciate how indicative it is of a serious central neurological problem, and how it can be used together with the presence of headache and neck pain to make a presumptive diagnosis of VBI and avoid moving the patient’s neck at all.
What Is Dizziness?
Dizziness is probably best defined as a sense of disequilibrium. It can include vertigo, oscillopsia, giddiness, wooziness, nausea, vomiting, light-headedness, and almost anything else the patient is pleased to call dizziness. This feeling of disequilibrium can be caused by problems in the organs responsible for sensing imbalance, the peripheral nervous system taking sensations to the central nervous system, and the central nervous system components that process the information. It can also be caused by visual and other inputs that impair the perception of balance — such as when a train slowly pulls out of a station so that the station appears to be moving, producing a very disorienting sensation that patients may describe as dizziness. Another example is motion sickness.
The term therefore requires categorization. The usual classification of dizziness is peripheral and central. Central dizziness can be defined as dizziness caused by impairment of the central neurological system that deals with balance — that is, the perception of perturbations in the center of gravity and the volitional and reflexive responses to such perturbations. Peripheral dizziness is, for the most part, caused by dysfunctional sensory organs of balance.
Central balance structures include the vestibular nuclei, vestibular tracts, thalamus, cerebellum, and neocortex. Peripheral structures include proprioceptive receptors in the extra-ocular muscles, the TMJ and its muscles, the entire spine and limbs, trunk muscles, and even pressure receptors on the soles of the feet. But probably the biggest influence on the sensation of dizziness comes from tissues closest to the head — the eyes (vision and proprioception from the muscles) and the upper neck, and to a lesser extent the TMJ.
Type 1, 2, and 3 Dizziness
This etiological classification of peripheral or central dizziness must be established from assessing the patient’s dizziness. So the precursor of the etiological diagnosis must be a symptom-based classification: Type 1, Type 2, or Type 3.
Type 1 dizziness is an illusion of movement — either vertigo (a spinning movement) or oscillopsia (a swaying or linear movement).
Type 2 is termed pre-syncope dizziness, after the feeling that you are going to pass out. It includes all forms of dizziness sensations that are not Type 1: giddiness, light-headedness, nausea, and so on.
Type 3 is not really dizziness as defined above but actually imbalance or disequilibrium.
To illustrate: if you spin around and around, the first sensation is Type 1, followed immediately by Type 2 (the regret that you did it), while during the Type 1 dizziness, Type 3 occurs as you stagger around trying to find your center. By comparing the patient’s symptomatology with the illness scripts of peripheral and central dizziness, we can start to make a clinical determination of the etiology and take appropriate steps — either refer out for more definitive diagnostic measures or continue with the examination.
Type 3 dizziness unassociated with Type 1 dizziness should be considered part of a neurological impairment, degeneration, or disease/injury to the central nervous system such as the cerebellum. When it is associated with Type 1 dizziness the problem may be of either central or peripheral origin.
Type 1 dizziness perhaps allows the clearest determination as to whether dizziness is due to central or peripheral lesions. By far the most common form of Type 1 dizziness is vertigo, and its most common direction is around a vertical axis if upright or a coronal axis if lying. However, it can be around a sagittal axis so that the patient feels as if somersaulting forwards or backwards — and this is so unusual that you should probably consider the cause to be central.
Labyrinthine vs. Central Vertigo
| Labyrinthine | Central | |
|---|---|---|
| Intensity | Severe | Moderate (VBI may be severe) |
| Persistence | Non-persistent | Persistent (VBI: 20 min–20 hrs) |
| Axis | Vertical, sometimes coronal | Vertical; may be sagittal |
| Direction consistency | Consistent | May alternate |
| Neurological symptoms | None (may have blurred vision) | May be present; with VBI usually not |
| Neurological signs | Nystagmus (appropriate for VOR disturbance) | May have variable signs, mostly related to lateral medullary syndrome |
Type 2 Dizziness
Type 2 dizziness is much less clear in pretty much all respects. There is no clear operational definition as there is with Type 1, and it may include any of the following and more:
- Wooziness
- Giddiness
- Light-headedness
- Nausea
- Vomiting
- Unsteadiness
- Faintness
- Weird feeling
In fact, anything the patient relates as dizziness is dizziness. The intensity and timelines that apply to Type 1 do not apply here. But severe dizziness and prolonged persistence may indicate more serious causes. Anything lasting more than 15–20 minutes should be viewed with suspicion, especially if it is not improving or is worsening. This is where a neurological examination becomes essential — at a minimum, a cranial nerve exam should be carried out. If positive, the patient must be transported to the emergency room.
Causes of Dizziness
These are multiple and extensive:
- Middle and inner ear problems including Meniere’s disease, viral infection, acoustic neuropathy, canalolithiasis/cupulolithiasis (BPPV), labyrinthine concussion (temporal bone fracture, traumatic hydrops, fracture/dislocation of the ossicles, rupture of the tympanic membrane, oval window), middle and inner ear infections
- Migraine
- Circulatory problems including orthostatic hypotension, cardiac arrhythmias, myopathy, failure, and attacks
- Neurological conditions such as MS can lead to progressive loss of balance
- Cerebellar pontine tumors
- Metabolic disorders including anemia and hypoglycemia
- Medications — approximately 400 drugs list dizziness as an adverse effect, including most of those our patients take such as NSAIDs and analgesics
- Age — older patients are more likely to have problems with balance due partly to degenerative changes and also the higher likelihood of developing a medical condition that causes dizziness
- Spondylogenic dizziness caused by a conflict in messages between the components of balance from cervical dysfunction — well known to us but rarely mentioned in the literature
The pathologies that will mainly concern us in this essay are:
- Traumatic VBI
- Vestibular dysfunction
- Spondylogenic dysfunction
It would appear from the literature that dizziness is somewhere between 95–100% sensitive for traumatic VBI, and that the dizziness may be either Type 1 or Type 2. Type 1 dizziness can usually be fairly easily classified as central or peripheral — but regardless, it needs to be evaluated by a specialist.
Clinical Red Flags
As with most things, basing a diagnosis on a single symptom is not the best idea except where that symptom is pathognomonic of the condition. It is very necessary that other symptoms and tests are integrated into the process. But some of these tests may be dangerous if the patient is suffering from VBI — and it may well be that the subjective examination will contraindicate any movement testing. This applies particularly to conditions where movement could be disastrous: especially VBI and high cervical fracture.
Be wary of the following:
- Sudden traumatic onset of severe occipital pain and dizziness
- Central vertigo
- Sagittal plane vertigo (somersaulting sensation)
- Prolonged or severe Type 2 dizziness
- Progressive dizziness
- Dizziness and blurred vision
In all of these cases it would probably be best to avoid movement tests — the so-called vertebral artery tests and ROM tests. A cranial nerve examination (CNX) while the patient is dizzy, if possible, is the best approach. If the patient is not currently dizzy or if the CNX is negative, integrate the behavior of the dizziness with the behavior of the headache and neck pain to associate or disassociate the symptoms.
Subjective Dizziness Flowchart
The following flowchart outlines a suggested approach to the subjective assessment of dizziness in isolation from other subjective questions or physical tests, except for the CNX. In clinical practice the examination is not isolated to dizziness but includes its relationships with neck pain, headache, and the results of other physical tests. Regardless of how these other tests pan out, a patient recommended for the ER should go to the ER.
VBI Series
- VBI Screening: Why the 5 Ds Fail Physical Therapists
- Vertebrobasilar Anatomy for Physical Therapists
- VBI and Dizziness: Clinical Guide for Physical Therapists (this article)
Jim Meadows, BScPT, MCPA, FCAMPT
Jim Meadows is a physiotherapist with over 50 years of clinical and educational experience, having trained in England in 1972 before building a career spanning England, Norway, and Canada. He holds a Diploma in Physiotherapy from the Prince of Wales’ School of Physiotherapy in the UK, a BSc in Physical Therapy from the University of Alberta, and a Fellowship in the Canadian Academy of Manipulative Physiotherapy (FCAMPT).
For 12 years, Jim served as chair of the Canadian Orthopaedic Division’s Education and Specialization Committees, and was a past Examiner and Instructor with the Division. He is a co-founder and Senior Examiner with the North American Institute of Orthopaedic Manual Therapy (NAIOMT), and serves as President and Director of Curriculum at IMPACT — the Institute of Manual Physiotherapy and Clinical Training. His spinal manipulation course has graduated approximately 900 physiotherapists across Canada and the United States.
Jim is the founder of Swodeam, an online resource for clinical essays on manual therapy and musculoskeletal physiotherapy, and the author of Orthopedic Differential Diagnosis in Physical Therapy: A Case Study Approach and a companion manual therapy video series. His essays are preserved on Physical Therapy Web with his permission.
