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|Posted on 15 February, 2012 at 3:37||comments (12)|
This is an information leaflet available to my patients and does not imply that this is appicable to you or your Consultan'ts practice. Not everyone would agree with all the statements made here, so if you have this condition, or think you have, you need to consult your own doctor.
An Information Leaflet
What is Trigeminal Neuralgia?
This is a condition, which is characterised by very severe facial pain. it is worse than a labour pain - I'm told. The particular features of this condition are that the pain is almost always confined to one side of the face and it occurs out of the blue without any obvious cause and does not go away by itself in thelong term.
Trigeminal Neuralgia is diagnosed mainly from the patient’s story. The pain typically occurs on one side of the face and may involve the upper, middle or lower thirds of the face, sometimes two thirds of the face and occasionally the whole of one side.
The character of the pain is that it is a very sharp pain, often described as feeling like ‘ red hot needles ‘ and the jabs of pain last for seconds or minutes and are of sudden onset. The pain may occur so suddenly that it can make the patient jump when it occurs.
Another feature of Trigeminal Neuralgia is that there is often a trigger spot on the face or in the mouth which if touched can start the pain off. The pain can also be provoked by touch, cold, washing the face, eating and talking. Unfortunately this can drive patients to despair and some patients loseweight and may even avoid social contact.
You do not need to have all of these features to have Trigeminal Neuralgia but usually most of them are present. Dull pain that spreads across the mid-line of the face and does not have typical provoking features is not Trigeminal neuralgia. If you have doubts about the type of pain that you are suffering, discuss this with your consultant.
We do not know for certain what the underlying cause of this painful condition may be. There are however theories about the cause, which seem to fit the facts and offer a chance of long-term treatment.
The nerve that supplies one half of the face and part of the scalp comes from the lower part of the brain at the back. It is thought that where the nerve enters the brain (the Root Entry Zone) a blood vessel lies incontact with the nerve and this ‘vascular compression’ causes the pain.
This seems to be correct as the vast majority of patients that we operate upon do have this problem, inthis area. Unfortunately only 90% ofpatients do have a demonstrable vessel causing the pain at operation so we arenot 100% certain that our theory is correct.
There are other causes of Trigeminal Neuralgia such as pressure from tumours or inflammatory conditions of the nervous system but most of these other causes can be excluded by doing abrain scan before planning treatment.
Treatment of TrigeminalNeuralgia is divided up into medical and surgical treatment.
The mainstay of medicaltreatment is to give drugs that are normally used in the treatment ofepilepsy. These particular drugs slowdown nervous tissues ability to transmit the electrical impulses, which allowsnerves to function. The most effectiveof these is Tegretol (carbamazepine) which can be prescribed in doses up to1200 milligrams / day. Other drugs suchas Epanutin (phenytoin) and Epilim (sodium valproate) can also be used. Usually the pain is controlled by a smalldose of Tegretol and other treatment is not needed, as this drug is usuallywell tolerated and safe for long-term use. The other drugs tend to be used if the patient does not tolerate theTegretol for one reason or another. Ifthe drugs don’t work there are surgical options that can be considered.
A number of surgicalprocedures are available each with particular advantages anddisadvantages. Your surgeon will be ableto tell you which is the most suitable treatment in your individual case.
There are four basic waysto treat this condition:
1. A needle is placed under local or sometimes a generalanaesthetic into the area where the nerve comes out of from the skull usingx-ray control. A small amount ofglycerin is then injected after which the patient has to keep still with thehead held forward for about 5-6 hours to allow the glycerin to do it’s job (notall surgeons feel that keeping the head still in this way is necessary). It works by dehydrating the nerve and causingit mild damage and this reduces its ability to transmit pain. This is a good treatment but the effects lastonly from 6 to 24 months usually.
2. Instead of injecting anything into the nerve an electricalneedle can be inserted into the nerve and used to cauterize the nervepartially. The needle placement is mademore precise by being able to stimulate the nerve to produce a gentle tingleand when this is in the place where the patient has the pain that particularportion of the nerve can be heated up electrically. This is a good treatment but suffers from thedisadvantage that it leads to a degree of permanent numbness of the face andalso a kind of after pain can result (in 5-10%) which can be very difficult totreat. It does however give good longterm relief of pain and only 15-20% of patients get the pain back in the longterm.
3. The nerve can be cut. This is usually done by an open operation and usually results incomplete facial numbness on that side of the face. This is only ever done as a last resort asthe numbness of the eyeball that results can produce serious problems withvision in the long term.
4. The above treatments all work by damaging the nerve and theonly treatment that we have which is non-destructive is an operation called ‘micro-vascular decompression’.
Microvascular decompression is a relatively new operation that has been used now for about thirty years. A small opening is made at the back of the skull and the edge of the brain is gently lifted aside. The Trigeminal nerve is identified and usinga microscope is examined for contact with a blood vessel, which is gentlylifted away from the nerve and held away with a special tiny sponge.
This effectively stops the pain in more than 97% of cases and leads to a permanent cure in approximately 90% of patients. Thisoperation has the advantage that it is very effective and does not damage the nerve and return of the pain is rare. Numbness following surgery is usually temporary however 15% of patients get some permanent loss of feeling in the face.
Shortly before admissionto hospital, it is likely that you will be seen in a pre-admission clinic whereyour general fitness for the anaesthetic is assessed. You may need a chest x-ray, ECG (a hearttracing) and some blood tests.
When you are admitted to hospital, surgery is usually carried out the following day. Most patients are given an injection or tablets before surgery to relax them (pre-med). The anaesthetist who puts you to sleep will visit the day before surgeryto decide on this and on your general fitness for the anaesthetic.
On the day of surgery you will be taken to the anaesthetic room in the operating theatre and given an injection to make you sleep during the operation, after which you will awaken on the Neurosurgical Ward.
Microvascular decompression is generally a safe procedure and can be carried out at almost any age. The oldest patient operated on in Middlesbrough with this operation was aged 89 and did extremely well!
You can expect to be in hospital for a minimum of five days, unless some complication arises. One of the risks of this operation is that when manipulating blood vessels in the base of the brain a stroke might occur. We have not had such a case in the last 10 years however.
Occasionally the fluid, which bathes the brain, can leak into the wound and require a further small operationto repair the defect in the brain's coverings. This is an uncommon event but should your wound leak any fluid or othermatter following surgery it is important to inform your doctor.
Because other nerves are close to the Trigeminal nerve they can be affected by the surgery. This is very rare but there have been cases of weakness in the muscles of one side of the face temporarily, temporary double vision, temporary unsteadiness when walking and mild deafness on the side of the operation.
On your return home you are unlikely to feel like doing your own cooking cleaning or shopping for at least a few weeks. It is important thatyou should have a friend or relative staying with you during that time to look after you during your convalescence. If this is impossible, discuss the matter with the ward sister in the pre-assessment clinic or when you are admitted to the ward.
Following the surgery you should not be in any severe pain. If youare, you should consult your GP or telephone the ward.
If the wound becomes red, painful, tender or swollen or discharges any matter it is important you should either telephone your GP or the ward.
The wound will either have staples to close the skin or a dissolvable stitch buried under the skin. Ask the ward staff to advise you about this before you go home, as the staples should be removed between five and sevendays. You should avoid the wound getting wet during the first week after surgery. However, if the wound becomes wet when you wash your hair for example, you are unlikely to come to any harm and it can just be dabbed dry with a clean towel.
Most patients have returned to normal activities such as work and driving between six weeks and three months but this varies according to the patient’s age.
A normal sex life can beresumed within two or three weeks.
If the surgery is successful you can say goodbye to the anti-convulsant drugs as soon as youawaken after the operation.
|Posted on 2 February, 2012 at 5:28||comments (0)|
Here's an article 'wot I rote' on Whiplash injury of interest to patients, lawyers etc:
(Excuse the word spacing - cut and paste isn't too good on this website!)
Fred Nath FRCS
The term Whiplash injury is probably one of the most misused terms of all the medical terminology. The layman, some health professionals and the majority of lawyers use it incorrectly. This is because whiplash is a specific term thatrefers to a specific mechanism of injury and has characteristic pathological consequences.
To fit the definition, a whiplash injury must be an injury where there is a rear shunt motor vehicle accident, which pushes the recipient forwards. The head lags behind and the neck therefore may sustain an extension injury.The head is then thrown forwards and a flexion injury occurs. As the body falls back there is a further insult to the neck as the head is flung back again. A better term would be acceleration / deceleration injury as it describes what happens better. Most of the subsequent symptoms occur because of injury to the small joints of the spine (1), (9).
This is a different injury from that sustained by the driver of the vehicle behind,who is predominantly thrown forwards and the extension component to the neck (where the head is thrown back) is minimal by comparison. Flexion injuries particularly if combined with a degree of rotation are far more likely to resultin intervertebral disc lesions than a simple whiplash injury. In such injury there is always a degree of twisting strain as the loading on the neck is never perfectly symmetrical in a forwards / backwards direction at the time of impact. There are therefore twisting elements to the injury, which act upon the ligaments in the neck to increase the likelihood of disc prolapse.
The typical clinical picture in whiplash injury is that following the injury there is no obvious immediate pain. In severe cases there may be rapidly developing stiffness of the neck. Initially function is not impaired either. The patient may proceed from the accident to continue with daily activities but begins to notice stiffness in the neck. The following night is often uncomfortable and the majority develop significant pain and stiffness by the subsequent morning.This clinical picture varies considerably from patient to patient according to the severity of the original accident and whether the patient has a vulnerable neck by reason of pre-existing degenerative changes, which may give rise to symptoms after injury.
The severity of the injury is determined by many things (8). The posture at thetime of the accident may be such that there is twisting of the neck if the patient is looking to the side. Whether a seat belt is worn, whether there is a headrest, the springiness of the seat back, the angle of the seat back, theheight of the patient, the force of impact and the muscle tension (13) at the moment of impact may all be implicated in the evolution of the subsequent clinical picture. It follows therefore that the speed of the impact or the damage to the vehicle are not a good guide to the severity of the injury in this type of clinical picture, however, there is research suggesting minimum speeds at which injuries can occur (3). Whiplash injuries therefore are more complex than one might think at first glance, and it is unwise to group all the patients together, hence many of the studies published on whiplash injury vary considerably in their findings in relation to outcome.
Delay Before Symptoms:
Whiplash injury most commonly results in stretching of ligaments ( the sinews which hold the joints together) and muscles. The affected tissues may be torn in a severe injury but most commonly the injury is mild or moderate and serious mechanical damage to the neck is uncommon. This stretching of the tissues leads to bleeding (on a small scale) and an acute soft tissue inflammatory reaction. The inflammatory response takes time to appear as it is akin to the tissues' reaction to infection. When developing an infection (e.g. a common cold) the symptoms tend to evolve rather than happen instantaneously because it takes time for the inflammatory response to occur.
Soft tissue trauma therefore, takes time to produce symptoms. A typical case with a mild to moderate degree of trauma may take up to a few days to appear and to begin with, may be masked by painkilling medication taken to treat other injuries. It is therefore not uncommon for the patient to start to complain of stiffness and discomfort in the neck up to a week later. The delay in the appearance of the symptoms often leads the unwary to suppose that there is no connection between the injury and the development of the symptoms.
A swith any soft tissue injury, there are acute symptoms giving rise to initial acute pain and stiffness in the neck and this phase may last up to a few months following the trauma. There is then a secondary phase when the symptoms are intermittent and mild. The secondary phase may last up to two years, although some studies suggest that improvement in symptoms may continue for longer (7).Exacerbations caused by specific activities, which can last for days at a time,occur commonly. Soft tissue injuries of this type however, are not likely to give rise to symptoms after two years (at the outside) and the vast majority of whiplash injuries do not give symptoms for more than a few weeks.
Although the most common effect of a whiplash injury is to cause injury to the neck, there may be other associated injuries.
Anterior Neck Symptoms:
As thehead is thrown back the muscles at the front of the throat and neck are stretched. It is therefore common for the patient to complain of pain at thefront of the neck. This is particularly likely if at the moment of impact thepatient clenches the jaw. Much of the force of the extension injury will beabsorbed by the muscles at the front leading to tearing of muscle fibres and short-term pain. I personally have never seen a case in which there were severe symptoms at the back of the neck as well as the front, because of the bracing effect of the two opposing muscle groups upon each other.
Significant tearing of muscles at the front of the spine behind the gullet (oesophagus) may also lead to soft tissue swelling and mild difficulty swallowing. This is unusual however, without a fracture or dislocation of the bones in the neck.
Head Injury Symptoms:
In Neurosurgical circles it is well known from experimental pathology studies involving sudden acceleration of the head that severe injury to the brain can occur even without an impact. The rationale behind this is that as the head is thrown forwards, the brain shifts inside the skull, and if this is very sudden, it can result in shearing of long white matter nerve tracts inside the brain. This leads to significant damage in specific areas. The experimental studies required very forceful flexion / rotation acceleration and sudden deceleration of a severity that is not mirrored by the common whiplash injury,however it is well known and described that symptoms akin to post-concussionalsyndrome may occur linked with whiplash injury even when there is no actual impact of the head. This is also supported by the fact that cognitive deficits such as poor memory and concentration are also described in whiplash injury.
Jawpain (temporo-mandibular dysfunction):
As the muscles at the front of the neck contract they can pull on the lower jaw. The joints between the jaw- bone (mandible) and the lower side of he skull can therefore be pulled upon forcibly. This can lead to local pain in the jaw joint, which can lead to uneven movement of the jaw when opening the mouth or chewing. The patient may get into the habit of opening the mouth in an uneven fashion and this leads to a variety of symptoms including pain on eating and clicking of the jaw when opening the mouth.
The suddenness of the impact or the apparent inevitability when seeing the approaching vehicle in therear-view mirror, may lead to significant subsequent fear and anxiety. Such anxiety may be expressed in the form of typical post-traumatic stress symptoms (flash-backs, symptomatic anxiety in motor vehicles, nightmares and panic attacks) or may lead to subsequent depression exacerbated by unemployment and other social ill effects of the sequelae of the injury. Such depression may lead to a lengthening of litigation even in a no-fault compensation system(4). That post-traumatic stress occurs with whiplash injury, is well documented but the severity of this and the length of time for which it occurs is logically most likely to be a reflection of pre-morbid personality and previous history.
The vast majority of patients experience a few weeks of significant discomfort inthe neck which may be accompanied by tingling in the fingers and radiation ofthe pain to the back of the head. There is then a phase when the symptoms become intermittent. If there is background degenerative disease in the neck however, there may be associated symptoms with significant radiation to the upper limb due to nerve root irritation, neurological symptoms in the arms such as numbness and weakness, and significant headache (radiating upwards from theneck to the back of the head and sometimes over the vertex of the head tobehind the eyes). These patients do not do well, and in a small percentage, there may be chronic pain that never settles. The number of patients with symptomatic complaints varies considerably in different studies, ranging from 35% (11) to 70% at 15 years from injury (2) and 58% at 5 years in another study.
Psychological effects of the injury may alter the whole clinical picture. The sudden and unexpected nature of the injury may produce a degree of mental shock or post-traumatic stress and there may be anxiety and depression associated. It has been shown in a research study that certain groups of people have a higher resistance to the psychological effects than others (12). It is of interest that this study showed doctors to be more resistant to long-term symptoms than non-doctors, suggesting that if the subject is not as worried about the ill effects of the symptoms then they have less effect.
There is usually an indication of a psychological effect from the expert's examination however; as such patients often exhibit signs of functional overlay. This may take the form of pain with vertical pressure on the head or non-anatomical patterns of numbness or observing the patient moving the headn ormally in conversation but having very restricted movement on examination.There is no particular reason to expect these signs to indicate purposeful simulation, which in the author's experience is rare.
The vast majority of patients experience a few weeks to months of acute pain thatbecomes intermittent then fades gradually into insignificance unless there are associated features on clinical evaluation to suggest either more severe injuryor degenerative disease symptomatology.
A small proportion of patients continue with significant neck symptoms and whiplash associated disorders on a permanent basis. This has been the subject of much study but the causal evidence is conflicting. On the one hand, there are studies that suggest that psychological factors play a large part in the continuation of symptoms (6). On the other hand, there are studies to suggest that prolongation of the litigation is related to the chronicity of the clinical picture. It is therefore difficult to know how to assess such studies particularly as the definition of the type of injury is variable and the exact mechanism of injury varies somewhat from case to case, It may be better to assess each individual case for additional factors such as the occurrence of degenerative disease which will influence the time scale of symptoms. It seems likely that this is the main separating factor between those who have a short time course and those with permanent symptoms.
Thee arly management may also influence the outcome, as the use of collars to immobilise the neck early on after injury will produce stiffness in the joints and may have a negative effect upon the eventual outcome. Early mobilisation and gentle exercise and massage are probably the best treatments rather than keeping the neck still.
Thereis evidence to suggest that up to 7% of patients suffering whiplash injuries do not return to their previous employment (5), although one must consider that is especially likely in heavy manual workers.
Another factor that may influence the severity of the effects of whiplash injury is the time it takes for the court case to be settled. Those in whom the case is settled quickly have less pain for a shorter duration. This suggests that anxiety or other psychological factors, common in litigation, may have a negative effect upon the severity of the symptoms (4).
The term whiplash injury should be confined to rear shunt injuries. The injury itself commonly has delayed effects and may engender symptoms similar to head injury and psychological consequences as well as symptoms in the front of the neck and jaw. The biomechanics of the injury itself suggest that it is complex and multifactorial and it is suggested that each case should be assessed on it's merits against the background of the previous history of the patient sinceoutcomes vary so much.
(1)BogdukN. Yoganandan N. Biomechanics of the cervical spine Part 3: minor injuries. [see comments.]. [Review]Clinical Biomechanics. 16(4):267-75, 2001May
(2)Borchgrevink GE. Lereim I. Royneland L. Bjorndal A. Haraldseth O. National health insurance consumption and chronic symptoms following mild necksprain injuries in car collisions. Scandinavian Journal of Social Medicine. Vol24(4) (pp 264-271), 1996.
(3)Castro WH. Schilgen M. Meyer S. Weber M. Peuker C. Wortler K. Do"whiplash injuries" occur in low-speed rear impacts?. European SpineJournal. 6(6):366-75, 1997.
(4)Cote P. Hogg-Johnson S. Cassidy JD. Carroll L. Frank JW. The association between neck pain intensity, physical functioning, depressive symptomatology and time-to-claim-closure after whiplash. Journal of Clinical Epidemiology.54(3):275-86, 2001 Mar.
(5)GozzardC. Bannister G. Langkamer G. Khan S. Gargan M. Foy C. Factors affecting employment after whiplash injury. Journal of Bone & Joint Surgery - BritishVolume. 83(4):506-9, 2001 May.
(6)Obelieniene D. Schrader H. Bovim G. Miseviciene I. Sand T. Pain after whiplash: a prospective controlled inception cohort study. Journal ofNeurology, Neurosurgery & Psychiatry. 66(3):279-83, 1999 Mar.
(7)Olivegren H. Jerkvall N. Hagstrom Y. Carlsson J. The long-term prognosis of whiplash-associated disorders (WAD). European Spine Journal. 8(5):366-70,1999.
(8)Ono K. Kanno M. Influences of the physical parameters on the risk to neck injuries in low impact speed rear-end collisions. Accident Analysis &Prevention. 28(4):493-9, 1996 Jul.
(9)Siegmund GP. Myers BS. Davis MB. Bohnet HF. Winkelstein BA. Mechanical evidence of cervical facet capsule injury during whiplash: a cadaveric study using combined shear, compression, and extension loading. Spine. 26(19):2095-101,2001 Oct 1.
(10)Squires B. Gargan MF. Bannister GC. Soft-tissue injuries of the cervical spine.15-year follow-up. Journal of Bone & Joint Surgery - British Volume. Vol78(6) (pp 955-957), 1996.
(11)Soderlund A. Lindberg P Long-term functional and psychological problems in whiplash associated disorders. International Journal of Rehabilitation Research. Vol 22(2) (pp 77-84), 1999
(1)Virani SN. Ferrari R. Russell AS. Physician resistance to the late whiplash syndrome.Journal of Rheumatology. 28(9):2096-9, 2001 Sep.
(12) Winkelstein BA. Nightingale RW. Richardson WJ. MyersBS. The cervical facet capsule and its role in whiplash injury: a biomechanical investigation. Spine. 25(10):1238-46, 2000 May 15.