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Trigeminal Neuralgia
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Trigeminal Neuralgia: 

Cranial nerves exit from the base of the brain instead of the spinal cord (below). 

www.mhhe.com





There are 12 cranial nerves. The trigeminal nerve is one of these nerves. 

http://www.lhsc.on.ca/Health_Professionals/CCTC/edubriefs/thrdl1.htm



Trigeminal neuralgia (nerve pain) occurs when the trigeminal nerve is compressed or irritated. Pain will be felt in the cheek, forehead, nose, sinuses, lips teeth jaw, etc. The pain comes on suddenly and is intense. The trigeminal nerve supplies most of the feeling to the face and the innervates the jaw muscles. The most common cause of nerve compression is by the Superior Cerebellar Artery. 

www.painclinic.org



As the Superior Cerebellar Artery compresses the nerve, the nerve becomes irritated and hypersensitive to light touch, vibration, temperature and position sensors in the jaw muscles. A trigger is something that starts a neuralgia episode. Triggers include: light touch, applying something hot and cold to the face and dental work. The pain is usually one sided and occurs more in women. Trigeminal neuralgia is particularly nasty because it interferes with daily activity such as eating, swallowing, brushing teeth. Eating, washing, and touching your face. Treatment for trigeminal neuralgia includes medications, surgery and injections. The most common surgical procedure is microvascular decompression (MVD). In MVD the Superior Cerebellar Artery is teased away from the Trigeminal Nerve and a barrier is placed between the two.

Microvascular decompression surgery 
www.neurosurgery.ufl.edu/patients/trigeminal-neuralgia.shtml 





More General info on trigeminal neuralgia and atypical trigeminal neuralgia:

Trigeminal neuralgia (TN), tic douloureux (also known as prosopalgia, the Suicide Disease or Fothergill's disease) is a neuropathic disorder characterized by episodes of intense pain in the face, originating from the trigeminal nerve. It has been described as among the most painful conditions known. It is estimated that 1 in 15,000 people suffer from TN, although the actual figure may be significantly higher due to frequent misdiagnosis. In a majority of cases, TN symptoms begin appearing after the age of 50, although there have been cases with patients being as young as three years of age. It is more common in females than males.

The trigeminal nerve is a paired cranial nerve that has three major branches: the ophthalmic nerve (V1), the maxillary nerve (V2), and the mandibular nerve (V3). One, two, or all three branches of the nerve may be affected. 10-12% of cases are bilateral (occurring on both the left and right sides of the face). The pain may be felt in the ear, eye, lips, nose, scalp, forehead, cheeks, teeth, or jaw and side of the face.

TN is not easily controlled but can be managed with a variety of treatment options.

The disorder is characterized by episodes of intense facial pain that last from a few seconds to several minutes or hours. The episodes of intense pain may occur paroxysmally. To describe the pain sensation, patients may describe a trigger area on the face so sensitive that touching or even air currents can trigger an episode; however, in many patients the pain is generated spontaneously without any apparent stimulation. It affects lifestyle as it can be triggered by common activities such as eating, talking, shaving and brushing teeth. Wind, high pitched sounds, loud noises such as concerts or crowds, chewing, and talking can aggravate the condition in many patients. The attacks are said by those affected to feel like stabbing electric shocks, burning, pressing, crushing, exploding or shooting pain that becomes intractable.

Individual attacks usually affect one side of the face at a time, lasting from several seconds to a few minutes and repeat up to hundreds of times throughout the day. The pain also tends to occur in cycles with remissions lasting months or even years. 10-12% of cases are bilateral, or occurring on both sides. This normally indicates problems with both trigeminal nerves since one serves strictly the left side of the face and the other serves the right side. Pain attacks are known to worsen in frequency or severity over time, in some patients. Many patients develop the pain in one branch, then over years the pain will travel through the other nerve branches. Some patients also experience pain in the index finger.

It may slowly spread to involve more extensive portions of the trigeminal nerve. The spread may even affect all divisions of the nerve, and sometimes simultaneously. Cases with bilateral involvement have not indicated simultaneous activity. The following suggest a systemic development: rapid spreading, bilateral involvement or simultaneous participation with other major nerve trunks. Examples of systemic involvement include multiple sclerosis or expanding cranial tumor. Examples of simultaneous involvement include tic convulsive (of the fifth and seventh cranial nerves) and occurrence of symptoms in the fifth and ninth cranial nerve areas.

Outwardly visible signs of TN can sometimes be seen in males who may deliberately miss an area of their face when shaving, in order to avoid triggering an episode. Successive recurrences are incapacitating and the dread of provoking an attack may make sufferers unable to engage in normal daily activities.

Some patients report continuous pain or continuous pain during waking hours; for reasons that are not yet known, TN sufferers rarely have pain attacks or are awakened due to pain while they are sleeping. In fact, most patients have a very brief window of reprieve upon awakening from sleep, though that window can sometimes last only minutes. The mechanisms as to why one feels no pain while they are asleep, or in a slumber state, even though a pillow may be in contact with a "trigger point" on one's face, remains a mystery to physicians and dentists.

There is also a variant of TN called atypical trigeminal neuralgia (also referred to as "trigeminal neuralgia, type 2"),[10] based on a recent classification of facial pain. In some cases of atypical TN the sufferer experiences a severe, relentless underlying pain similar to a migraine in addition to the stabbing shock-like pains. In other cases, the pain is stabbing and intense but may feel like burning or prickling, rather than a shock. Sometimes the pain is a combination of shock-like sensations, migraine-like pain and burning or prickling pain. It can also manifest as an unrelenting, boring, piercing pain.

The trigeminal nerve is a mixed cranial nerve responsible for sensory data such as tactition (pressure), thermoception (temperature), and nociception (pain) originating from the face above the jawline; it is also responsible for the motor function of the muscles of mastication, the muscles involved in chewing but not facial expression.

Several theories exist to explain the possible causes of this pain syndrome. It was once believed that the nerve was compressed in the opening from the inside to the outside of the skull; but newer leading research indicates that it is an enlarged blood vessel - possibly the superior cerebellar artery - compressing or throbbing against the microvasculature of the trigeminal nerve near its connection with the pons. Such a compression can injure the nerve's protective myelin sheath and cause erratic and hyperactive functioning of the nerve. This can lead to pain attacks at the slightest stimulation of any area served by the nerve as well as hinder the nerve's ability to shut off the pain signals after the stimulation ends. This type of injury may rarely be caused by an aneurysm (an outpouching of a blood vessel); by a tumor; by an arachnoid cyst in the cerebellopontine angle;[12] or by a traumatic event such as a car accident or even a tongue piercing.

Short-term peripheral compression is often painless, with pain attacks lasting no more than a few seconds. Persistent compression results in local demyelination with no loss of axon potential continuity. Chronic nerve entrapment results in demyelination primarily, with progressive axonal degeneration subsequently. It is, "therefore widely accepted that trigeminal neuralgia is associated with demyelination of axons in the gasserion ganglion, the dorsal root, or both." It has been suggested that this compression may be related to an aberrant branch of the superior cerebellar artery that lies on the trigeminal nerve. Further causes, besides an aneurysm, multiple sclerosis or cerebellopontine angle tumor, include: a posterior fossa tumor, any other expanding lesion or even brainstem diseases from strokes.

A large portion of multiple sclerosis patients have TN, but is not a symptom of MS. Only two to four percent of patients with TN,[citation needed] usually younger,[citation needed] have evidence of multiple sclerosis, which may damage either the trigeminal nerve or other related parts of the brain. It has been theorized that this is due to damage to the spinal trigeminal complex. Trigeminal pain has a similar presentation in patients with and without MS.

Postherpetic Neuralgia, which occurs after shingles, may cause similar symptoms if the trigeminal nerve is damaged.

When there is no [apparent] structural cause, the syndrome is called idiopathic.

As with many conditions without clear physical or laboratory diagnosis, TN is unfortunately sometimes misdiagnosed. A TN sufferer will sometimes seek the help of numerous clinicians before a firm diagnosis is made.

There is evidence that points towards the need to quickly treat and diagnose TN. It is thought that the longer a patient suffers from TN, the harder it may be to reverse the neural pathways associated with the pain.

The dentist must ensure a correct diagnosis does not mistake TN as a temporomandibular disorder. Since triggering may be caused by movements of the tongue or facial muscles, TN must be differentiated from masticatory pain that has the clinical characteristics of deep somatic rather than neuropathic pain. Masticatory pain will not be arrested by a conventional mandibular local anesthetic block.

Dentists who suspect TN should proceed in the most conservative manner possible and should ensure that all tooth structures are "truly" compromised before performing extractions or other procedures.

Atypical Trigeminal Neuralgia (ATN), or Type 2 Trigeminal Neuralgia, is a rare form of Trigeminal neuralgia, a disorder of the fifth cranial nerve. This form of neuralgia is difficult to diagnose, as it is rare and the symptoms overlap with several other disorders. The symptoms can occur in addition to having migraine headache, or be mistaken for migraine alone, or dental problems such as Temporomandibular joint disorder, musculoskeletal issues, and hypochondriasis. ATN can have a wide range of symptoms and the pain can fluctuate in intensity from mild aching to a crushing or burning sensation, and also to the extreme pain experienced with the more common trigeminal neuralgia.

ATN pain can be described as heavy, aching, stabbing and burning. Some sufferers have a constant migraine-like headache. Others may experience intense pain in one or in all three trigeminal nerve branches, including teeth, ears, sinuses, cheeks, forehead, upper and lower jaws, "behind" the eyes, and scalp. In addition, those with ATN may also experience the shocks or stabs found in type 1 TN.

Many TN and ATN patients have pain that is "triggered" by light touch on shifting trigger zones. ATN pain tends to worsen with talking, smiling, chewing, or in response to sensations such as a cool breeze. The pain from ATN is often continuous, and periods of remission are rare. Both TN and ATN can be bilateral, though the character of pain is usually different on the two sides at any one time.

Both forms of Facial Neuralgia are relatively rare, with an incidence recently estimated between 12 and 24 new cases per hundred thousand population per year.

ATN often goes undiagnosed or misdiagnosed for extended periods, leading to a great deal of unexplained pain and anxiety. A National Patient Survey conducted by the US Trigeminal Neuralgia Association in the late 1990s indicated that the average facial neuralgia patient may see six different physicians before receiving a first definitive diagnosis. The first practitioner to see facial neuralgia patients is often a dentist who may lack deep training in facial neurology. Thus ATN may be mis-diagnosed as Tempormandibular Joint Disorder.

This disorder is regarded by many medical professionals to comprise the most severe form of chronic pain known in medical practice. In some patients, pain may be unresponsive even to opioid drugs at any dose level that leaves the patient conscious. The disorder has thus acquired the unfortunate and possibly inflammatory nickname, "the suicide disease".

Symptoms of ATN may overlap those of a dental problem called "Atypical Odontalgia" [literal meaning "unusual tooth pain"], with aching, burning, or stabs of pain localized to one or more teeth and adjacent jaw. The pain may seem to shift from one tooth to the next, after root canals or extractions. In desperate efforts to alleviate pain, some patients undergo multiple (but unneeded) root canals or extractions, even in the absence of suggestive X-ray evidence of dental abscess.

ATN symptoms may also be similar to those of Post Herpetic Neuralgia, which causes nerve inflammation when the latent Herpes Zoster virus of a previous case of Chicken Pox re-emerges in Shingles. Fortunately, Post-Herpetic Neuralgia is generally treated with medications which are also effective against ATN.

The subject of atypical trigeminal neuralgia is considered problematic even among experts. Some forms of orofacial pain are relatively well defined and easy to recognize while the others seem to represent a diverse group of pain syndromes with considerable overlap, several classification schemes, vague characterization and controversial entities. The term Atypical TN is broad and due to the complexity of the condition, there are considerable issues with defining the condition further. Some medical practitioners no longer make a distinction between facial neuralgia (a nominal condition of inflammation) versus facial neuropathy (direct physical damage to a nerve).

Due to the variability and imprecision of their pain symptoms, ATN or Atypical Odontalgia patients may be misdiagnosed with "Atypical Facial Pain" or "Hypocondriasis", both of which are considered problematic by many practitioners. The term "Atypical Facial Pain" is sometimes assigned to pain which crosses the mid-line of the face or otherwise does not conform to expected boundaries of nerve distributions or characteristics of validated medical entities. As such, the term is seen to comprise a diagnosis by reduction.

As noted in material published by the [US] National Pain Foundation: "Atypical Facial Pain is a confusing term and should never be used to describe patients with trigeminal neuralgia or trigeminal neuropathic pain. Strictly speaking, AFP is classified as a “somatiform pain disorder”; this is a psychological diagnosis that should be confirmed by a skilled pain psychologist. Patients with the diagnosis of AFP have no identifiable underlying physical cause for the pain. The pain is usually constant, described as aching or burning, and often affects both sides of the face (this is almost never the case in patients with trigeminal neuralgia). The pain frequently involves areas of the head, face, and neck that are outside the sensory territories that are supplied by the trigeminal nerve. It is important to correctly identify patients with AFP since the treatment for this is strictly medical. Surgical procedures are not indicated for Atypical Facial Pain."

The term "Hypochondriosis" is closely related to "Somatiform Pain Disorder" and "Conversion Disorder" in the Diagnostic and Statistical Manual (DSM-IV) of the American Psychiatric Association. As of July 2011, this axis of the DSM-IV is undergoing major revision for the DSM-V, with introduction of a new designation "Complex Somatic Symptom Disorder". However, it remains to be demonstrated that any of these "disorders" can reliably be diagnosed as a medical entity with a discrete and reliable course of therapy.

It is possible that there are triggers or aggravating factors that patients need to learn to recognize to help manage their health. Bright lights, sounds, stress, and poor diet are examples of additional stimuli that can contribute to the condition. The pain can cause nausea, so beyond the obvious need to treat the pain, it is important to be sure to try to get adequate rest and nutrition.

Depression is frequently co-morbid with neuralgia and neuropathic pain of all sorts, as a result of the negative effects that pain has on one's life. Depression and chronic pain may interact, with chronic pain often predisposing patients to depression, and depression operating to sap energy, disrupt sleep and heighten sensitivity and the sense of suffering. Dealing with depression should thus be considered equally important as finding direct relief from the pain.

Treatment of patients believed to have ATN or TN is usually begun with medication. The long-time first drug of choice for facial neuralgia has been Carbamazepine (Tegretol), an anti-seizure agent. Due to the significant side-effects and hazards of this drug, others have recently come into common use as alternatives. These include Oxcarbazepine (Trileptal), Lamotrigine (Lamictal), and Gabapentin (Neurontin). A positive patient response to one of these medications might be considered as supporting evidence for the diagnosis, which is otherwise made from medical history and pain presentation. There are no present medical tests to conclusively confirm TN or ATN.

If the anti-seizure drugs are found ineffective, the supervising physician may introduce one of the tri-cyclic anti-depressant medications such as Amitriptyline (Elavil) or Nortriptyline (Pamelor), among others. The tri-cyclic antidepressants are known to have dual action against both depression and neuropathic pain. Other drugs which may also be tried, either individually or in combination with an anti-seizure agent, include Baclofen, Lyrica, tranquilizers, muscle relaxants, and opioid drugs such as Percocet or Oxycodone.

For some ATN patients, treatment with opioid drugs may represent the only viable medical option which preserves quality of life and personal functioning. Although there is considerable controversy in public policy and practice in this branch of medicine, practice guidelines have long been available and published.

If drug treatment is found to be ineffective or causes disabling side effects for the patient, one of several neurosurgical procedures may be considered. The available procedures are believed to be less effective with Type II (Atypical) Trigeminal Neuralgia than with Type I (Typical or "classic") TN. Among present procedures, the most effective and long lasting has been found to be Micro-Vascular Decompression (MVD), which seeks to relieve direct compression of the Trigeminal Nerve by separating and padding blood vessels in the vicinity of the emergence of this nerve from the brain stem, below the cranium. Radio Frequency Rhizotomy has similar outcome statistics, with a different mechanism. Rhizotomy introduces a controlled lesion on the nerve distribution further downstream from the brain stem, to interrupt or moderate nerve response and over-sensitivity. Less effective forms of Rhizotomy include Balloon Compression and Glycerol Rhizotomy. Radiosurgery (Gamma radiation or electron beam) techniques — Gamma Knife or Cyber Knife — require no surgical incision. However initial results and persistence of results are not as good as for MVD or RF Rhizotomy.

Choice of a surgical procedure is made by the doctor and patient in consultation, based on the patient's pain presentation and health and the doctor's medical experience. Some neurosurgeons resist the application of MVD or other surgeries to Atypical Trigeminal Neuralgia, in light of a wide spread perception that ATN pain is less responsive to these procedures. However, recent papers suggest that in cases where pain initially presents as Type I TN, surgery may be effective even after the pain has evolved into Type II.