Weight LossPain Managementprinciples of treatmentdrug side effects




The sensation of balance is complicated.  Humans need a sophisticated balance mechanism.  As we walk on two legs with only a narrow base and a height that is many times that base width (just think of London buses), then it is essential that our brain knows in effect where we are in relation to the ground at all times. 

When we move our head and eyes, the world in effect remains as it is when our head is still.  If for some odd reason, we choose to stand on our hands or head, the world still remains the right way up.  Why is this?  If we spin round and round in circles, then we all know from childhood games that we will emerge from such play with feelings of dizziness and a tendency to fall over.  What we do under these circumstances is overwhelm the balance mechanism temporarily leading to our staggering or falling.  Some of us have better balance mechanisms than others.  This is in part genetic or it may come about by training.  Ballet dancers, skiers and mountain climbers for instance have particularly well-trained balance mechanisms that allow them to perform feats that most normal people are unable to achieve.



Our sensation of balance requires the integration of three different systems.  The first, and probably most important, is the so-called vestibular apparatus.  The second, our eyes and their ability to move.  The third comprises the position sense receptors of the whole of our axial skeleton but also position sense receptors in our pelvis, hip, knee, ankle and foot joints. 

Neural signals arise from each of these “systems”.  The signals arrive in the brain stem by passage along the peripheral nerves and then the spinal cord. Within the back part of the brain or the brain stem, these signals merge sending what is in effect a corporate message into the brain which allows us to recognise that we are sitting, standing, lying, moving, twisting, bending or any other movement that we care to challenge our biped state.

Most of the discussion will now focus on the vestibular apparatus although there will be some discussion about eye movements as well.



The vestibular apparatus consists of five sensory organs within a structure called the labyrinth.  The labyrinth is a system of cavities or semi-circular canals sitting within the petrous temporal bone of the skull.  These cavities contain the sensors for both the auditory, that is hearing, and vestibular (balance) systems.

There are two otoliths as well as three semi-circular canals on either side of the head. 

The otoliths have two functions.  They are able to sense the head’s linear motion.  What this means is the movement of the head forward or to the side.  They are also able to sense the position of the head in relation to gravity.  In simple terms, these organs are able to tell us which is up and which is down.  If we did not have otoliths, we would be in serious difficulty knowing what to do when we try to bend down or stand up as we would not know for certain where gravity was acting.

The semi-circular canals are able to sense angular acceleration due to head rotation and hence it is vital that the otoliths and the semi-circular canals work closely together in order to maintain our equilibrium.



The otoliths are spherical.  They are called the utricle and the saccule.  Part of these structures is covered with hair cells which project into a jelly-like substance.  Within this jelly, there are calcium carbonate crystals that allow for movement of the hair cells. 

In simple terms, motion is picked up by the otoliths.  The hair cells are bent by the calcium crystals and these cause chemical changes in the neural fibres that go to the hair cells which causes a nerve impulse to be generated in the 8th cranial nerve that transmits these impulses into the central nervous system.

It is often assumed that at rest, these nerve fibres are doing little but that is incorrect.  We know that in the passive state, there is a baseline firing rate of about 100 nerve action potentials every second.  This baseline firing rate will change according to the movements of the hair cells so that there will either be an increase or decrease in the firing rate.  Such changes in the firing rate tell the central nervous system what is going on with head movement.



We have three semi-circular fluid-filled canals on each side of the head.  The three canals are nearly at 90º to each other.  One canal is horizontal and the other two are known as the anterior and posterior canals.  At the end of each canal, there is a swelling called the copula.  The copula once again contains hair cells. 

With the head movement, the fluid in the semi-circular canals will lag behind that motion because of the inertia in any fluids.  This will cause a distortion within the copula which in turn will cause the hair cells to bend in one direction or the other.  This will then generate neural impulses in the vestibular division of the 8th cranial nerve.

As each canal sits at 90º to the other, then there will be more motion in one canal compared to the others on each side according to the rotation of the head.  The horizontal canal is sensitive to head rotation in the horizontal plane.  The right anterior canal is activated when the head tips as a combination of both nose and right ear down. As often happens in the body, the canals are arranged in pairs so that each canal on one side of the head has a twin canal on the other side.  When one of the canals is activated, then the canal that is its partner on the other side is maximally inhibited.  Although not so important in this discussion, for completeness I would mention that the anterior canal of one side has the posterior canal on the other side as its partner canal.



Nearly all of us are born with two eyes which are capable of moving up, down and side to side.  The eyes move in a conjugate way.  This means that when one eye moves in any particular direction, the other eye will follow in order to make sure that we continue to have binocular vision.  Those movements are generated by six muscles within the orbit on each side.  The movement of the eyes is quite separate to our ability to see.  If however there is an imbalance between the eye muscles or the three nerves that supply those eye muscles, then we will suffer with double vision.

The movement of the eyes is very important in the balance mechanism. The nerves going to the eye muscles are activated by structures known as the eye nerve nuclei within the brain stem. These nuclei are very closely opposed to the balance mechanism nuclei within the brain stem.  There are a lot of connections and pathways between the eye muscle nuclei and the balance mechanism.  As is explained later, when our balance mechanism does not work properly, we become much more reliant on so-called visual cues that enable us to continue with a reasonable sense of balance unless challenged by darkness or rapid head movements when visual cues are diminished or removed.  This then exposes the balance mechanism to a much greater challenge when individuals often fall over.  Older people who have visual disturbance will have much greater difficulty with their balance mechanism.  This and a general slowing of neural responses with age and wear and tear on the balance mechanism itself makes it much more likely that older people will fall.  When this is added to a whole range of reduced autonomic (automatic) neural deficiency and problems with arthritis and reduced position sense responsiveness in the axial skeleton, it is actually quite surprising that all of us do not keep falling down all the time as a consequence of the ageing process.



If there is a disturbance in the semi-circular canals or the otoliths, then there is a mismatch between the input information from these five end organs when the head is moved or turned.  The brain will interpret this mismatch as a sensation of rotation of the body or the environment.  When there is damage to the otolith organ, then a sensation of tilt or a feeling that the body is moving through the environment, will occur.  There are a number of other symptoms that can be generated by damage to the balance mechanism and these include a muzzy sensation, dizziness or a true vertigo, that is      a hallucination of movement, together with nausea and/or vomiting.  Nausea, vomiting and the need to lie down are usually more marked with peripheral lesions of the balance mechanism rather than central lesions sitting with the brain stem. 



When we move our head normally, the eyes rotate opposite to the head.  This in effect cancels the motion of the head.  Ballet dancers, gymnasts and acrobats are the best at this.  They are remarkably able to stabilise the image of what is going on around them within their retina.  We manage to stabilise the image on the retina by what is known as the vestibulo-ocular reflex (VOR).  This reflex means that the eyes rotate at the same speed as the head but in the opposite direction and this stops us having a blurring of the visual image which would be inevitable with head movement.  Just think of the energy and effort that goes into the taking of a photograph without blurring and yet every moment of our lives sees a similar phenomenon taking place and yet we have clear vision.

If we continue to move our head rapidly in the dark, the normal VOR will stop and the brain gets the false impression that there is not any movement.  If vision is then restored, there will be a sensation of movement and in turn there is a subjective symptom of dizziness.

Vision itself can generate the VOR (for neurologists this is known as the opticokinetic response).  This may generate a feeling that there is movement when for instance we look out of a car or plane window and an adjacent vehicle starts to move. 


With the eyes open and very rapid head movement, then there will be a high volley or neural signals arising from the different structures.  The visual signal however will take over the neural input as the vestibular mechanism tends to fatigue more readily in the normal state.

When the balance mechanism is damaged for any reason or if it is poorly trained or suffers as a consequence of prolonged recumbency or lack of use, then the imbalance between the visual pathway and the vestibular mechanism gets enhanced relative to the visual pathway. This means that there is a much greater vulnerability to the brain perceiving this imbalance as dizziness with even minor head movement rather than the rapid movement that would normally generate this. 

Motion sickness is an intriguing phenomenon. It is caused by the balance mechanism telling us that we are moving whereas the visual mechanism gets the perception that there is not such movement.  Different people will get more or less motion sickness according to many factors including a genetic predisposition and what would be regarded as a less trained interaction between the balance mechanism and the visual pathway.  For instance the best way to avoid motion sickness when on a boat is to go out on deck and let the visual pathway focus on the horizon so that the visual impulses are picking up the same message as the vestibular mechanism itself. 


Benign paroxysmal positional vertigo  (BPPV)

There are a number of disorders that affect the balance mechanism. There are of course a number of disease processes such as multiple sclerosis in younger people and cerebro-vascular disease in older individuals that can damage the central connections of the balance mechanism.  In clinical neurological practice however the most common causes of a balance mechanism disturbance are those that affect the peripheral mechanism.

Benign paroxysmal positional vertigo or BPPV is a common condition that does affect the balance mechanism.  Sometimes we do not know the cause.  It may reflect a viral infection or it can occur after trauma.  Acute attacks of vertigo as defined by an hallucination of movement take place associated with head movement.  The mechanism by which this disorder occurs is the presence of otoconial debris, that is calcium crystals that become displaced into one or occasionally more of the semi-circular canals.  Characteristically the attacks of vertigo are precipitated by movements or positioning within the plane of the affected canal.  The movement of the head causes this debris to move within the canal and this generates an abnormal stimulus of the ampullary crest on one side compared to the other.  This sends a differential signal through the brain stem via the vestibular nuclei which in turn is read by cortical structures in such a way that vertigo is appreciated even though of course the individual is not actually moving.  If one thinks about gentle waves lapping on the seashore on a sandy beach in a rhythmic fashion compared to the same scene with a large boulder then placed on the sandy shore, one would see that there will be turbulent flow around the large boulder which interrupts the smooth passage of water on to the beach.

People with BPPV report prolonged feelings of loss of equilibrium or just “not being right” between the more acute episodes.  It is increasingly being recognised that postural control is also impaired outside acute episodes.  The older the patient, then the worse the postural control and this has been shown by comparison to normal people without a balance disorder at different ages.

We know that the postural disturbance is more apparent for sixty days after the first attack of BPPV when the sufferer is more dependent on visual cues during this time.

Dynamic posturography is a form of testing that can be undertaken and it is apparent that the more commonly effective semi-circular canal in BPPV leads to greater postural impairment than those who have the rarer otoconial debris in the horizontal canal.  Even after therapeutic manoeuvres are carried out, the postural disorder remains particularly in the posterior canal group.  It may be that the residual postural disturbance is caused by residual debris in the posterior canal but this is not known for certain.

Individuals who have abnormal posture due to posterior canal involvement will show increased body sway in both the lateral and anterio-posterior planes compared to normal people. 

There is a treatment called the “Epley” manoeuvre which improves the lateral body sway but not the anterior-posterior sway with the latter returning to normal much more slowly but usually by three months after treatment.  When there is confirmed postural instability after an Epley manoeuvre, then ongoing vestibular rehabilitation will improve compared to an untreated group.  The key message for all people who have suffered BPPV from whatever cause including trauma is that the more one treats the condition with specialised therapists, then the more likely the better outcome with a good prognosis. 



Disorders of the balance mechanism can be investigated by vestibular function tests.  Although these tests are objective, they are limited in the way they can test the mechanism. 
The central nervous system is able to adopt a number of adapted mechanisms to cope with disturbances of the balance mechanism.  If there is a combination of damage to the balance mechanism together with damage to other parts of the nervous system such as the cerebellum, reticular formation of the brain stem or spinal cord as can occur in head injury, then the disability can be much greater.  This is because the compensatory mechanisms are less able to function.

Animal experiments have demonstrated that compensation from acute vestibular lesions is delayed and even limited by a period of immobilisation.  This means that patients with balance lesions should be mobilised at the earliest possible stage after an insult.  There are a number of techniques that can be used to treat balance disturbances.  It is useful with vestibular function tests to demonstrate whether the primary problem is in the peripheral or the central part of the balance mechanism. 

On the whole, peripheral balance mechanism disturbances carry with them a better prognosis and are more likely to respond to the so-called Epley manoeuvre.  All patients however will benefit from a programme of Cawthorne-Cooksey or Hallpike exercises shown by a physiotherapist who has been fully trained in balance rehabilitation.

Animal experiments have demonstrated that compensation by the nervous system from acute vestibular lesions is delayed and even limited or restricted by a period of immobilisation.  This means that like so much in recovery from illness or injury, there is no indication for rest and if anything rest or limited mobility is actually contra-indicated. 



As indicated above, there is an urgent need for balance rehabilitation soonest after acute vertigo with nausea or vomiting has passed.  There will be a natural compensation by the balance mechanism.  Equally there will be ongoing natural recovery from any insult or injury.

Where there has been damage or injury, there is a natural “velocity of recovery”.  That does vary from person to person but there is always a tendency to recover.  Psychological mechanisms and failure to mobilise for whatever reason will lead to significant ongoing functional handicap and that needs to be treated soonest.  If there is a significant emotional component, then the quicker that physical rehabilitation together with psychological support and possible pharmacotherapy introduced, then the better the final outcome.

Specific detail of the treatment is well covered on a number of websites.  The key terms are “balance rehabilitation”, “Epley manoeuvre”, “Cawthorne-Cooksey” and “Hallpike” rehabilitation exercises.

On the whole, there is no reason to use vestibular sedatives which if anything are contra-indicated in terms of sub-acute or chronic rehabilitation.  Medications such as Cinnarazine or Prochlorperazine or Betahistine may have a role in the acute management of vertigo.  Once that acute phase has dissipated, then these medications should be stopped and the appropriate rehabilitative physiotherapy continued. 

On the whole, the more that individuals do the balance exercise programme, then the better they get.  Those who do little or stop doing the exercise programme can expect to do less well and they will be a self-fulfilling prophecy as far as poor recovery is concerned. 

Frequently people with a balance disorder go on to develop a whole range of secondary problems. These may include benign headache.  This may represent migraine or tension type headache.  Neck muscle spasm is very common leading to neck pain and stiffness.  Anxiety and panic attacks because of the constant feeling of disequilibrium frequently manifest at presentation when in fact the diagnosis is a primary balance mechanism disturbance. 

From the writer’s perspective, it is remarkable how often he sees people within the medico-legal process who have suffered a significant head injury where the balance disturbance has just not been identified.  These individuals will have seen Accident and Emergency Department Doctors including specialists in that territory.  They will have seen Orthopaedic Surgeons who deal with their orthopaedic injuries.  They may well have seen Neuropsychologists, Neuropsychiatrists, Psychiatrists and Clinical Psychologists.  None of these individuals will necessarily have been trained in detecting a balance mechanism disturbance.  It is usually only when the Neurologist gets a chance to see the individual that the true mechanism of many of their symptoms is identified.

Unfortunately in Britain, very few people with head and underlying brain injury actually get seen by a Neurologist as part of the clinical process.  This is caused by the severe shortage of Neurologists who only have limited time in the District Hospitals where most head injury presents.