FACIAL NEUROPATHOLOGY OROFACIAL PAIN
A delta and C fibers are associated with pain In terms of velocity, most pain fibers have a slower velocity than the others.
PAIN FIBERS(PERIPHERAL NERVE FIBERS) • A-DELTA: • Responsible for temperature and fast or first pain. • Faster • Conduction velocity is 12-45 m/sec • Myelinated • C-FIBERS: • Responsible for slow or second pain, and temperature. • Is unmyelinated • Much slower • Conduction velocity is 0.2-2.0 m/sec • Odontogenic pain from pulp is associated with this
TYPES OF CUTANEOUS PAIN • 1. Pricking pain, which is felt rapidly. It is felt that pricking pain is mediated by A-delta fibers. A fibers also conduct touch, warmth, and cold • When you first feel the stick from a needle • 2. Dull, aching sometimes burning pain, which is mediated by C fibers. C fibers also conduct itch, warmth, and cold • Interplay between these nerve fibers to allow us to get into the CNS. All sensation from the face is mediated by the trigeminal nerve.
THE TRIGEMINAL SYSTEM • All sensory input from the face and mouth is carried by V (trigeminal). • Cell bodies of the trigeminal afferent neurons are located in the gasserian ganglion • Impulses carried by V enter directly into brainstem(pons) and synapse in the trigeminal spinal tract nucleus • Spinal tract nucleus responsible in most cases in significant pain
SPINAL TRACT NUCLEUS • Divided into 3 parts: A. the subnucleus oralis Significant for association with oral pain mechanisms B. the subnucleus interpolaris C. the subnucleus caudalis-predominates in trigeminal nociception Oralis and caudalis are the principle portions associated with pain
Remember: the spinal tract nucleus is most important in perception of facial pain
PRIMARY NEUROTRANSMITTERS FOR PAIN TRANSMISSION Glutamate - an amino acid Substance P – a peptide Substance P has been looked at in a lot of new papers coming out on pain. They are trying to find inhibitors for pain. We are starting to see a decrease in finding new pain relief mechanism because pharmaceutical companies don’t find it to be profitable. Bone pain and orthopedics and face pain are still heavily researched.
TISSUE INJURY:causes K+, bradykinin and arachidonic acid release Once you get prostaglandin release you will get nociception – this is almost always mediated by the primary afferent neuron
Release of Substance P cause release of histamine and serotonin(5HT), and more bradykinin Substance P is associated with histamine release. Bradykinin is a significant mediator of pain. That is why a substance P inhibitor stops the cascade.
Release of substance P, histamine, serotonin initiate more nociception One of the problems with pain is that pain sometimes causes a change in the brain. The brain is plastic, you have to make sure you stop pain. Giving patients appropriate pain meds is important. If you cause primary hyperalgesia the patient will have a special tract that will cause high grade pain from non-nociocous stimuli. Many of these patients have to undergo trigeminal cutting in order to stop the pain. The problem with that is numbness of the face.
PAIN EXPERIENCE • Involves the psychologic (past experiences, cultural behaviors and emotional state) and • Physiologic aspects(involves the transduction,transmission and modulation of pain) • The experience of pain is linked to emotional,behavioral, and cognitive phenomena If you have psychology associated with the physiology, it is much more difficult to treat it. It is common to use antidepressants with narcotics to address that. Whether you use tricyclics or SSRIs is up to the practitioner.
EVALUATION OF MAXILLOFACIAL PAINSENSORY DYSFUNCTION • Obtain a chief complaint and include onset, clinical course since onset, intensity and location • Ask for assessment by the pt for objective/subjective descriptors i.e. is dysfunction intermittent/continuous; character of pain (throbbing, deep, area/face feel wooden); does it occur in relation to other functions (with function or spontaneous); precipitants or reliever of sxs; associated sxs etc
Pain that wakes the patient up in the middle of the night is usually real pain. You have to be willing to treat or refer the patient.
DESCRIPTORS OF ALTERED SENSATION • Numb • Tingling • Wet • Rubbery • Stretched • Swollen • Crawling • Itching • Prickling • Electric • You have blood flow but you have transmission that is affected • Tender • Painful • Burning • Very problematic because it is hyperalgesia • If it gets here you will probably have to section the nerve to make it stop • If you don’t you will probably have to put the patient on anti-seizure medications to make it stop To the right is bad descriptors
INSPECTION / EXAMINATION • Skin changes in color or texture • More pitted and more pallor • Atrophic changes • Iatrogenic induced trauma • If the patient is numb the will probably have areas where they have bit their tongue • Decreased/altered taste (affected lingual nerve), difficulty in chewing • Difficulty in speaking or facial animation • Difficulty speaking is usually associated with the lingual nerve
Axis 1 – somatic pain, like TMJ, pulp pain, headaches Neuropathic pain – Trigeminal, Glossopharyngeal, Geniculate, all the neuralgias Also the pain associated with herpes and burning mouth The worst ones are CRPS and SMP Metabolic neurapathies also fall under this Axis 2 – psychologic problems Mood disorders, anxiety disorders, PTSD These processes can influence axis 1, you may need to use polypharm to treat this population
AXIS I (PHYSICAL CONDITIONS) • Cutaneous and mucogingival pains • Mucosal pains of the pharynx, nose, and paranasal sinuses • Pains of the musculoskel. Structures of the mouth/face • Pains of the visceral structures of mouth/face • Pains of the neural structures of mouth/face
AXIS II (PSYCHOLOGIC CONDITIONS) • Anxiety disorders • Mood disorders • Somatoform disorders • Other conditions, such as psychologic factors affecting a medical condition PSYCHOLOGIC INTENSIFICATION OF PAIN
Patients who have pain will typically have elevated BP, pulse rate, and respiratory rate Always do a good exam because you are looking for trigger points and referral pain pattern.
FACIAL NEURALGIAS • Trigeminal Neuralgia • Glossopharyngeal Neuralgia • Geniculate Neuralgia • Superior Laryngeal Neuralgia • Occipital Neuralgia
NEURALGIA: Defined as paroxysmal, intermittent pain confined to specific nerve branches Not continuous, almost always associated with specific nerve branches
TRIGEMINAL NEURALGIA • Characterized by severe recurrent episodic attacks of unilateral pain distributed over a branch or, after many years, more than one branch of V. Associated with trigger zones • Incidence per 100,000: 2.7 men and 5.0 for women • Pain usu. in V-2 or V-3 in 60% of pts. • More often on Rt side of body • 70% of pts over the age of 50
Notes from the Last Slide • YOU WILL SEE THIS AGAIN • Almost always unilateral • It can have more than one branch associated with it • By definition, it has a trigger zone • It may be something as simple as hair touching your face or the wind • More prevalent in women • Where is the pain? The pain is in the distribution of the 2nd and 3rd division and more often on the right side of the body. • It is usually seen a woman over the age of 50. • This is a horrible disease, the patients are miserable and don’t want to stay doped up all the time.
TRIGEMINAL NEURALGIA • KEY: No sensory/motor loss • Everything is intact • Compression or distortion of the nerve root by an aberrant arterial loop • 2-4% of cases of TN have MS • TX: 1.Anti-Epileptic Drugs: Gabapentin,baclo- fen,lamotrigine,carbamazepine,oxcarbamazepine 2.SURG:Radiofrequency thermolysis, Microvascular nerve root decompression (requires opening up of the skull),Gam- ma knife radiation One cause is that they think on occasion you have an arterial blood vessel sitting on top of a nerve root. Must look at the liver enzymes when you use gabapentin Problem with invasive neurosurgery to treat = you have to cut the branch so you knock out the whole 2nd or 3rd division.
VASOGLOSSOPHARYNGEAL NEURALGIA • Rarer than trigeminal neuralgia • Charac. by unilateral paroxysmal stabbing pain in the posterior 1/3 of the tongue, pharynx,larynx, and soft palate. Cranial nn IX & X involved • Pain assd. with trigger zone, talking and swallowing usual stimulus • Bradycardia, hypoten., and syncope seen from activation of X • Tx: tegretol or phenytoin, topical anesthesia of pharyngeal mucosa
POST-ZOSTER NEURALGIARAMSAY HUNT SYNDROME • Herpes zoster is a self-limiting dz • M=F in frequency; 65% over age 70n • Syndrome arises from geniculate gangliositis. This results in a)facial paralysis, b)loss of taste of anterior 2/3 of tongue , c)loss of lacrimation, d)vesicular eruption of the external ear and e)severe pain in EAC
RAMSAY HUNT CON,T • Pain in the ear is severe and paroxysmal • Pain persists for weeks to years after eruption disappears • Herpes zoster (shingles) is the consequence of reactivation of the latent varicella-zoster(also causes chickenpox) virus.
POSTHERPETIC NEURALGIA-TRIGEMINAL GANGLIA • Similar syndrome as Ramsay Hunt except inflammation of the trigeminal ganglion by herpes zoster. • The dermatomal distribution is now associated with V-1, V-2, or V-3, and is associated with viral reactivation • 10-15% of cases, reactivation is in the ophthalmic division (ophthalmic zoster)
POST HERPETIC NEURALGIA • TX:Acyclovir, famciclovir, or valaciclovir. Result in more rapid resolution of cutaneous lesions and decreased viral shedding. Famciclovir associated with accelerated resolution of postherpetic neuralgia
SUPERIOR LARYNGEAL NEURALGIA • The superior laryngeal nerve is a br. of the Vagus, innervates the cricothyroid muscle. Will see periodic, unilateral submandibular pain radiating through eye, ear, and shoulder. Similar to IX neuralgia • Provoked by swallow/turn of the head/sneezing/yawning/nose blowing
OCCIPITAL NEURALGIA • The greater occipital nerve is a continuation of the C2 nerve and innervates the posterior scalp. • Will feel paroxysmal pain in posterior occipital region and cervical region
ATYPICAL FACIAL PAIN • Usually is a dx. of exclusion • Pain does not follow anatomic distribution of the Trigeminal nerve, crosses the midline and not limited to sensory distribution of a single nerve • More common than trigeminal neuralgia • 4th-5th decade; F>M; classified as a)psychogenic b)organic c)indeterminate
HEADACHES • Types: 1) Tension a)episodic or b)chronic. The chronic type may have a duration of 5 years or longer in 75% of pts. Tx with antidepressants(tricyclic)or NSAIADs 2)Vascular a)Migraines:paroxysmal headache lasting 24-72 hrs, usually unilateral. Frequency variable and aura or prodrome may precede
HEADACHES CON’T • 2-a) Migraines con’t: 80% of pts with family history. In childhood M>F, but after menarche F>M. Tx with compression of temporal artery, cold compress, biofeedback,narcotics. 2-b: Cluster also called Horton’s headache. 8X more common in men. May see family aggregation. Last from 15 min to 2 hrs but may occur 5-10x a day, periorbital in location and unilateral. Tx:Lithium, O2, intranasal lidocaine spray
HEADACHE CON’T • 3)Temporal arteritis, is an inflammation of medium- and large-sized arteries. Usually involves a branch of the carotid artery, but is a systemic dz, and may involve arteries in multiple locations. Occurs over the age of 55, F>M, and associated with polymyalgia rheumatica. Complex of fever,anemia, high ESR and HA. Tx with steroids.
NERVE INJURIES-CAUSATION • Inferior alveolar: Fractures of mandible, BSSO, 3rd molar removal, resection of mand.,preprosthetic surgery, implant- nerve repositioning procedures • Lingual: 3rd molar removal, resection, salivary gl. Removal, fracture and repair of mand. Angle fxs
NERVE INJURY CLASSIFICATION • Seddon: neuropraxia, axonotmesis, and neurotmesis • Sunderland: 1st through 5th degree