Halmagyi & Cremer, Assessment & Treatment of Dizziness
Journal of Neurology, Neurosurgery & Psychiatry
J Neurol Neurosurg Psychiatry 2000;68:129-134 doi:10.1136/jnnp.68.2.129
Assessment and treatment of dizziness
G M HALMAGYI,
P D CREMER
- Professor G M Halmagyi, Department of Neurology, Royal Prince Alfred Hospital, Camperdown, NSW 2050, Sydney, Australia email [email protected]
“There can be few physicians so dedicated to their art that they do not experience a slight decline in spirits when they learn that their patient’s complaint is giddiness. This frequently means that after exhaustive enquiry it will still not be entirely clear what it is that the patient feels wrong and even less so why he feels it.” From W B Matthews. Practical Neurology. Oxford, Blackwell, 1963.
These words are not quite as true today as when Bryan Matthews wrote them nearly 40 years ago. There is now cause for cautious optimism. Recent clinical and scientific developments in the study of the vestibular system have made the clinician’s task a little easier. We now know more about the diagnosis and even the treatment of conditions such as benign paroxysmal positioning vertigo, Menière’s disease, acute vestibular neuritis, migrainous vertigo, and bilateral vestibulopathy than we did in 1963 and our purpose here is to introduce the clinician to facts worth knowing.
(A) The patient who has repeated attacks of vertigo, but is seen while well
IS IT VERTIGO ?
”Doctor I get dizzy”. This is of course one of the most common problems encountered in office practice and the one to which Matthews was alluding. The clinician’s first job is to sort out whether the dizzy patient is having attacks of vertigo, or attacks of some other paroxysmal symptom. So what is vertigo and what are its mechanisms and clinical characteristics?
The first point about vertigo is that it is an illusion of rotation and that it is always due to asymmetry of neural activity between the left and right vestibular nuclei. This is true whether the vertigo is induced by being spun around and then suddenly stopped, whether it is induced by having cold water squirted in one ear, whether it is induced by otoconial particles rumbling up and down a semicircular canal duct, or whether it is induced by infarction of one vestibular nucleus. The second point is that vertigo is always temporary. Even after the vestibular nerve on one side has been surgically severed, the terrible vertigo and nystagmus that follow will always abate within a few days, not because the vestibular nerve has reanastomosed but because profound neurochemical changes have taken place in the brainstem during the process of vestibular compensation.
The third point is that vertigo is always made worse by head movement, just as angina is always made worse by exertion. If you don’t believe this, then try the following: spin yourself around about 10 times (standing or sitting, it doesn’t matter) and then stop and throw your head backwards, quickly.
Convinced? One can be reasonably sure then that the patient who is happy to move around while dizzy does not have vertigo, and that the patient who is dizzy all the time and whose dizziness is not made better by keeping still, either hasn’t got vertigo or hasn’t got the story right. Now that we are sure that our patient has vertigo the next question to answer is whether the vertigo attacks are spontaneous or positional. But before we go on to answer that let us consider briefly the diagnosis of other common paroxysmal disorders such as syncope, seizure, hypoglycaemia, and hyperventilation.
Obviously patients with aural vertigo should not lose consciousness but it is surprising how few people can give a confident and convincing answer to the simple question: “Did it feel like you were losing your balance or like you were losing consciousness ? Did it feel like you were going to pass out or fall over ?” Patients with vertigo might actually lose consciousness if they have been vomiting a lot, or if they had an otolithic drop attack and a head injury on the way down. Witness descriptions are not much help in identifying vertigo, but can be essential in identifying seizures and syncope. (Convulsive syncope is of course more complicated.) Tilt table testing, particularly with lots of invasive instrumentation, is, according to some, too sensitive and insufficiently specific to help much with the diagnosis of vasovagal (now renamed “neurocardiogenic”) syncope.1 2 Cardiac syncope can, particularly in a patient without heart disease, be a difficult diagnosis. An event monitor which the patient wears for several weeks is more useful, particularly for picking up intermittent heart block, than a 24 hour Holter monitor which is best at disclosing the asymptomatic arrhythmias. A cardiac electrophysiological study is good at picking up the sort of tachyarrhythmias that can cause syncope and is less irksome than an endless sequence of inconclusive indirect investigations. Video-EEG monitoring has proved helpful in the diagnosis of seizures but is not easily available to everyone. Measurement of blood glucose during an attack, possible with a finger-prick glucometer, is the easiest and most direct way to make the diagnosis of hypoglycaemia, something that is easy to miss in the patient who is not being treated for diabetes.
Whereas panic attacks, especially with hyperventilation, commonly cause a sense of dizziness that is not actually vertigo, patients with recurrent undiagnosed vertigo can develop panic attacks particularly if the vertigo attacks are reassuringly put down to “… just a little anxiety”. This is one of those unusual situations in which patients do as they are told: they go on to develop anxiety, panic, and even agoraphobia.3 “Phobic postural vertigo” is a variant of this problem in which patients, often with obsessive-compulsive personalities, complain of a mild subjective disturbance of balance while standing or walking, with momentary illusions of motion.4 The symptoms usually occur in specific places or in specific situations, and are associated with a distressing anxiety. Many cases follow a clear, well documented peripheral vestibulopathy. Not everyone likes the name “phobic postural vertigo”,5 although we all see these patients, and typically they do well with simple non-judgmental support and an accurate non-patronising explanation.6
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