Orofocial Pain

  • According to International Association For Study of Pain [IASP] 1994“Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage”.
  • According to Mohneim’s “Pain is defined as an “unpleasant emotional experience usually initiated by a noxious stimulus and transmitted over a specialized neural network to the central nervous system where it is interpreted as such”.
  • Allodynia: Is pain due to a stimulus that does not normally produce pain.
  • Hyperaesthesia: Is an increased sensitivity to stimulation and does not imply a painful sensation, but rather an augmented response to a specific sensory mode. (e.g. Touch, vibration, temperature)
  • Hyperpathia: Is a painful syndrome with increased reaction to a stimulus and an increased threshold, faulty identification and localization of stimulus, delayed and radiating sensation and after sensation may be present
  • Causalgia: Is a syndrome of burning pain, allodynia and hyperpathia after a traumatic nerve lesion and is often combined with vasomotor and sudomotor {sweat sensation} dysfunction and later trophic changes.
  • Hypoaesthesia: Decreased sensitivity to stimulation
  • Hypoalgesia: Special case of hypoaesthesia in which pain response to a normally painful stimulus is diminished.
  • Neuralgia: Pain in the distribution of nerve.
  • Neuropathy: Disturbance of function or pathologic change in a nerve.
  • Nociceptors: Are peripheral receptors preferentially sensitive to noxious stimuli.
  • Paraesthesia: An abnormal sensation, whether spontaneous or evoked {not unpleasant}
  • Dysesthesia: An unpleasant abnormal sensation.
  • Anesthetic Dolorosa: Paradoxic pain in a region of sensory loss following an injury to a cranial nerve or a nerve root  {seen often after surgical treatment of trigeminal ganglion / root for neuralgia}
  • Central Pain: Pain associated with a lesion of central nervous system.

  S.No

Cranial Nerve

Function

  I

Olfactory

Sense of smell

  II

Optic

 

Visual acuity, visual fields

  III

Oculomotor

Movement of eyeball, pupil and upper eyelid

  IV

Trochlear     

Eye movement

  V

Trigeminal

Tactile facial sensation, motor innervation ofmuscles of mastication, corneal reflex

  VI

Abducens

Lateral movements of the eyes

  VII

Facial

Movements of facial muscles extrinsic andintrinsic ear muscles taste (anterior two thirds oftongue)

  VIII

Acoustic Vestibular

Hearing, equilibrium and orientation of head inspace

  IX

Glossopharyngeal

Elevation of palate, movement of pharynx andlarynx. General sensation from palate, posteriorone third of tongue and oropharynx. Taste fromposterior one third of tongue and oropharynx.

  X

Vagus

Muscles of soft palate, base of tongue, pharynx,larynx. Parasympathetic fibres to thoracic andabdominal viscera

  XI

Accessory 

 

Movement of sternocleidomastoid and trapezius

muscles

  XII

Hypoglossal 

Movement of tongue

Pain can be classified:

  • Acute and chronic.
  • Somatic, neuropathic and psychogenic pain.
  1. Acute pain:
  • Unpleasant sensation.
  • Sudden onset, normal healing time required to overcome the causative mechanisms.
  • Respond predictably to traditional approaches.
  1. Chronic pain:
  • Defined by a perseverance of pain for longer than 6 months.
  • Beyond the typical time for healing; not self-limiting.
  • May be refractory to traditional modalities that require a multidisciplinary approach.
  1. Somatic pain: Abnormal stimulation of normal neural structures results in somatic pain.The clinical characteristics of pain that originates in superficial structures are distinctly different from those of deep origin.
  2. Neuropathic pain: Structural abnormality in the nervous system leads to neuropathic pain.
  3. Psychogenic pain: It arises from psychic cause, there is no obvious physiologic or natural source for this type of pain.

According to type of tissue system from which pain originates:

Intracranial or extracranial, musculoskeletal, neurovascular and neurogenous.

  1. Intracranial (within the skull) or extra cranial (outside of the skull) pain includes Idiopathic pain (Atypical facial pain, Atypical odontalgia, Burning mouth syndrome).
  2. Musculoskeletal pain– Arising from masticatory muscle disorders, Tempromandibular joint dysfunction and Tension-type and Cervicogenic (neck origin) headaches,
  3. Neuropathic pain– Thiscan be episodic or continuous in nature, Neurovascular pain, Psychogenic pain and pain associated with other diseases eg. Dental decay and abscess, periodontal disease, tumours,ulcers in the mouth, xerostomia, trauma, distant pathology (referred pain),systemic diseases, etc.
  1. Superficial somatic pain
    • Bright stimulating quality.
    • Precisely located by the patient.
    • Site of pain identifies the correct location of its source.
    • Involved in acute pain.
    • No secondary manifestations.
    • Arrested by topical application of anesthesia at the site of pain.
  2. Deep somatic pain
  • Dull, deep and depressing quality.
  • Arises from deeper body structures.
  • Site of pain may not always indicate the true source of pain.
  • Involved in chronic orofacial pain.
  • Exhibits secondary manisfestations like lacrimation, local edema or referred pain to other structures.

Nervous system controls all the activities of the body. Primarily, nervous system is divided into two parts:

  1. Central nervous system.
  2.  Peripheral nervous system.

Central nervous system (CNS) includes brain and spinal cord. It is formed by neurons and supporting cells called neuroglia. Structures of brain and spinal cord are arranged in two layers, namely gray matter and white matter.

Peripheral nervous system (PNS) is formed by neurons. It consists of cranial nerves, arising from brain and spinal nerves, arising from the spinal cord. It is again divided into two subdivisions:

  1. Somatic nervous system
  2. Autonomic nervous system. 
  1. Somatic Nervous System

Somatic nervous system is concerned with somatic functions.It includes the nerves supplying the skeletal muscles. Somatic nervous system is responsible for muscularactivities and movements of the body.

  1. Autonomic Nervous System

Autonomic nervous system is concerned with regulation of visceral or vegetative functions. So, it is otherwise called vegetative or involuntary nervous system. Autonomic nervous system consists of two divisions, sympathetic division and parasympathetic division.

Fields has described that the subjective experience of pain arises by 4 distinct process:

  • Transduction.
  • Transmission.
  • Modulation
  • Perception.

Process by which noxious stimuli lead to electrical activity in the appropriate sensory nerve endings.

Refers to the neural events that carry the nociceptive input into the CNS for proper processing.

Transmission system:

  • Peripheral Sensory Nerve– Primary afferent neuron that carries the nociceptive input from the sensory organ into the spinal cord.
  • Second Order Neuron– Which carries the input to the higher centers.
  • Interaction– Of neurons between the thalamus cortex and the limbic system as the nociceptive input reaches these higher centers.

Modulation is ability of the CNS to control the pain transmitting neurons.

Perception is reaching of the nociceptive input to the cortex is perceptionswhich immediately initiate a complex interaction of neurons between the higher centers of brain.

  1. Peripheral sensitization:
    • Tissue damage results in an increased sensitivity of nociceptor at the siteof injury.
    • The nociceptors exhibit spontaneous activity, lowered threshold, increased responsiveness to subsequent noxious stimuli.
  2. Central Sensitization:
    • The increased nociceptive activity leads to an increased neuronal barrage into the CNS followed by functional changes in spinal cord and brain that contributes to persistant pain.

A nerve is a cord like structure to convey electrical and chemical impulses.

It consists of connective tissue sheath.

  • Epineurium– Encloses bundle of nerve fibers
  • Perineurium-Each nerve bundle surrounded by its own connective tissue sheath
  • Endoneurium– Within each bundle the nerve fibres areseparated by interstitial connective tissue
  • The neuron is made up of the cell body, the dendrites and the axon
  • The cell body provides nutrients to the cell.
  • The dendrites are multiple branching outgrowths from the cell body that are the main receptors for the neuron.
  • The dendrites provide for communication between adjacent neurons

The Axon is a single fiber that leaves the cell body to communicate with another neuron at a distant site. The axon is also called the nerve fiber and may extend from a few millimeters to as long as a meter

  • Unipolar
  • Bipolar
  • Multipolar

Impulses are carried from the dendrites down the axon by way of an action potential. An action potential begins with a sudden change from the resting negative potential to a positive membrane potential & then ends with almost equally rapid change back to the negative potential.

Action potential moves down the cell membrane until reaches the end of axon. Resting state of cell membrane is POLARIZED with a slight negative charge. When membrane becomes DEPOLARIZED, there is sudden permeability to sodium ions to flow into the interior of the axon. Rapid diffusion of potassium ions to exterior reestablishes the normal negative resting membrane potential, REPOLARIZATION of membrane.

Synapse is the junction between two neurons. It is not an anatomical continuation. But, it is only aphysiological continuity between two nerve cells.

  • Any artificial or false peripheral synapse.
  • Signifies abnormal or pathologic change.

Two types of synapses are there:

  • Chemical synapse: Found in CNS.
  • Electrical synapse: Found in cardiac and smooth muscle.

Neurochemicals that transmit impulses across the synaptic cleft.

  • Smaller (rapidly acting) molecules.
  • Larger (slow acting) molecules.
  1. Acetylcholine:
    • It is secreted by neurons present in motor cortex, basal ganglia, and bymotor neurons innervate skeletal muscle, preganglioic neurons of atonomic nervous system, postganglionic neurons of parasympathetic and some sympathetic nervous system.
    • It act as an excitatory effect on the postsynaptic neuron
  2. Norepinephrine:
    • It is secreted by neurons of brain stem and hypothalamus.
    • Highest concentration found in locus ceruleus of pons.
    • It act as an excitatory neurotransmitter.
  3. Glutamate:
    • It is an amino acid secreted by presynaptic terminals.
    • It is found in spinal cord dorsal horn associated with noxious input.
  4. Aspartate:
    • It is an amino acid secreted by presynaptic terminals of sensory pathways in dorsal horn
  5. Serotonin:
    • It is secreted by nuclei originating in the median raphe of brain system.
    • It is a monoamine released by blood platelets.
    • It is synthesized in CNS from L-tryptophan, a dietary essential amino acid.
    • It is released when nucleus raphe magnus in brain system is stimulated by sensory input.
    • Peripherally act as an algogenic agent for vascular pain syndrome.
    • In CNS, it act as a chemical in endogenous antinociceptive mechanism.
    • It reduces stimulation evoked excitation of nociceptive dorsal horn interneuron.
    • It provides global suppression or enhancement that enables nociceptive pathways to respond more effectively to incoming sensory information
  6. Gamma amino butyric acid:
    • It is secreted by neurons in spinal cord, cerebellum, basal ganglia and parts of Cortex.
    • It acts as an inhibitory effect on postsynaptic neuron.
  7. Glycine:
    • It is secreted by spinal cord and trigeminal spinal nucleus.
    • It act as an inhibitory transmitter.
  8. Dopamine:
    • It is secreted by neurons originating in substantia nigra and extends into basal ganglia.
    • It act as an inhibitory effect.
  9. Histamine:
    • It is a vasoactive amine derives from amino acid histadine.
    • It serve as a neurotransmitter in CNS.

They are neuropeptides.

  1. Substance P:
  • It is a polypeptide composed of 11 amino acid
  • It is released at central terminals of primary nociceptive neuron.
  • It acts as an transport substance found at distal terminals.
  • It act as an excitatory neurotransmitter for nociceptive impulses.
  • It is released from unmyelinated afferent involved in neurogenic inflammatory
  • It is high in severely inflamed joints.
  1. Endorphin:
  • They are polypeptides (chains of amino acid).
  • They behave like morphine and bind to morphine receptors to obtund pain.
  • It is longer lasting requires the passage of latent period before it becomes active.
  • It has high antinociceptive potency.
  • It contributes to pain threshold and pain tolerance.
  1. Bradykinin:
  • It is endogenous polypeptide consisting of chain of 9 amino acids.
  • It is released as a part of an inflammatory reaction.
  • It is a powerful vasodilator and increased capillary permeability.
  • It acts as an algogenic agent that excites all types of receptors.
  • It requires presence of prostaglandins to act.
  • It released during ischemic episodes.

Oral sensations include:

  • The perception of touch, temperature, moisture [and possibly texture] at the surface of the oral mucosa.
  • Pressure and kinesthetic sensation in the deeper tissues.
  • Pain in both deeper and superficial location.
  • Taste with in oral cavity.

Oral sensations are mediated by:

  • The somatic sensory branches of cranial nerves V, VII, IX, X and of cervical spinal nerve  C1 To C3.
  • Afferent of cervical sympathetic nerves associated with cranial blood vessels.
  • Special sensory fibers for taste carried in branches of cranial nerves VII, IX, X.
  • Pain sensation might also be carried in cranial parasympathetic fibers in branches of III, V, VII, IX.
  1. Pulpal Pain
    • Quality varies depending on the status of the pulpal tissues (vital or nonvital).
    • Presence of an identifiable cause (caries, fracture, restoration, mechanical abrasion).
    • Tends to get better or worse but rarely remains the same over time.
    • Poorly localized
  2. Periodontal pain
    • Dull aching or throbbing.
    • Presence of an identifiable periodontal condition (periodontal pocket, abscess).
    • Discomfort often felt when biting pressure is released rather than while it is sustained.
    • Precisely localized.
  • If input is carried by an A-delta fiber it may synapse with a dynamic range of neurons and the higher centers by the way of neospinothalamic tract. This input is carried quickly to higher centers and is referred as Fast Pain.
  • If input is carried by C-fiber it synapses with a nociceptive specific neuron and is carried up paleospinothalamic tract.This tract passes through reticular formation and is influenced by many modulating interneurons. Nociception carried on this tract is called Slow Pain.
  • Deep somatic pain that emanates from muscles, bones, joints, tendons, ligaments and soft connective tissue bear a close relationship to the demands of biochemical function. Such pain yields a graduated response.
  • Visceral structures are innervated by high threshold receptors so that the pain is usually not felt until the threshold level is reached. No graduated response to noxious stimulus and are less responsive to biochemical function. 
  • Sensory fibers innervate the anterior part of the face, teeth, mucous membranes of the oral and nasal cavities, conjunctiva, dura mater of the brain, and intracranial and extracranial blood vessels.
  • Motor fibers supply the muscles of mastication.

Theories of pain are based on documented experimental evidence that neural impulses are altered, changed or modulated as they travel up the neuraxis to the higher centers.It is important to consider the various factors that influence the inhibition and excitation of painful experience.

  • Specificity theory.
  • Pattern theory.
  • Gate control theory
  • Descartes in 1664 described the pain system as a straight through channel from skin to brain. This theory proposes a direct, invariant relationship between pain perception and intensity of the stimulus.
  • Although much pain results from noxious stimulation it can occur from nonnoxious stimuli as well as spontaneously when there is no stimulus at all. Causalgia and neuralgia provide a dramatic refutation of the concept of a fixed direct line nervous system.

Proposed by Gold Scheiders in1894,pattern or summation theory proposed that particular pattern of nerve impulses that evoke pain are produced by the summation of skin sensory input at the dorsal horn cells. Fundamental assumption of pattern theory is that all cutaneous qualities are produced by spatial and temporal pattern of nerve impulses rather than separate modality specific transmission proposed by specificity theory.

Psychologist Ronald Melzackand the anatomist PatrickWallproposed the gate control theory for pain in 1965 toexplain the pain suppression.According to them, the pain stimuli transmitted byafferent pain fibers are blocked by gate mechanismlocated at the posterior gray horn of spinal cord. If thegate is opened, pain is felt. If the gate is closed, pain is suppressed.

When pain stimulus is applied on any part of body, besides pain receptors, the receptors of othersensations such as touch are also stimulated.When all these impulses reach the spinal cord through posterior nerve root, the fibers of touch sensation(posterior column fibers) send collaterals to the neurons of pain pathway, i.e. cells of marginalnucleus and substantiagelatinosa.Impulses of touch sensation passing through these collaterals inhibit the release of glutamate andsubstance P from the pain fibers.This closes the gate and the pain transmission is blocked.

Pain cannot be measured objectively because it is a subjective experience. Pain measurement is a complex and controversial psycho physiologic subject.Broad categories of pain measurement methods:

  1. Subjective Report.
  2. Unidimensional Tools.
  • Visual analog scale.
  • Category scale.
  • Numeric rating scales.
  1. Multi Dimensional Tools
  • MPQ {Mc Gill Pain Questionnaire}.
  • Brief Pain Inventory.

VISUAL  ANALOG SCALE {VAS}

  • A common and simple method of rating pain.
  • It consists usually of a 10 cm line labeled at the ends with “no pain” and “worst pain imaginable”.
  • The patient indicates the pain magnitude by marking the line at appropriate point.
  • The distance along the line can then be measured and recorded for future comparison.

It is debatable that the VAS represents ordinal (discontinuous) data or interval (continuous) data as it seems to lie somewhere in between. It provides more than a simple rank ordering {ordinal values} but equal distance between unit {interval} values cannot be assured.

The four point “none, mild, moderate and severe” scale is acceptable for recording pain magnitude, but number need to be assigned to each level ( 0,1,2,3) to quantify the data.

Scales from 0 to 10 is useful, except for the patient who responds “11”.When unidimensional rating scales are used alone, the score does not reflect the emotional and affective qualities of pain.Attempts have been made to overcome this problem in two ways:

  • By use of separate VAS ratings for the sensory and affective dimensions of pain.
  • By including the emotional and affective qualities of pain in aQuestionnaire.
  • It is also known as McGill pain index.
  • Developed at McGill University by Melzack and Torgerson in 1971.
  • It is a self-report questionnaire that allows individuals to give their doctor a good description of the quality and intensity of pain that they are experiencing.
  • 78 pain adjectives are arranged into 20 groups that are further arranged into sets of words describing sensory aspects, which are further arranged into sets of words describing sensory aspects of the quality of pain.

Orofacial pain can be classified into following different categories:

  1. Neuralgias
  • Primary Trigeminal Neuralgia (Tic Douloureux).
  • Secondary Trigeminal Neuralgia (CNS Lesion or facial trauma).
  • Herpes Zoster.
  • Post Herpetic Neuralgia.
  • Geniculate Neuralgia (Cranial Nerve VII).
  • Glossopharyngeal Neuralgia (Cranial Nerve IX).
  • Superior Laryngeal Neuralgia (Cranial Nerve X).
  • Occipital Neuralgia.
  1. Pain of musculoskeletal origin
  • Cervical Osteoarthritis.
  • Temporomandibular joint disorders.
  • TMJ Rheumatoid arthritis.
  • TMJ Osteoarthritis.
  • Myofacial Pain Dysfunction.
  • Fibromyalgia.
  • Cervical Sprain or Hyperextension.
  • Stylohyoid (Eagle’s) Syndrome.
  1. Primary vascular disorders
  • Migraine with aura.
  • Migraine without aura.
  • Cluster Headache.
  • Tension-type Headache.
  • Hypertensive Vascular changes (Aneurysm, Emboli).
  • Mixed Headache.
  • Cranialateritis.
  • Carotodynia.
  • Thrombophlebitis.
  1. Psychogenic pains
  • Delusional/hallucinatory.
  • Hysterical/Hypochondriac.
  1. Generalised pain syndromes
  • Post-traumatic pains.
  • Sympathetically maintained pain (Causalgia).
  • Phantom Pain.
  • Central Pain.
  1. Lesions of the ear, nose, and oral cavity
  • Maxillary Sinusitis.
  • Otitis media.
  • Odontalgia.
  • Dentin defects.
  • Pulpitis.
  • Periapical pathology/Abscess.
  • Cracked tooth/restoration.
  • Atypicalodontalgia.
  • Periodontal pathology.
  • Occlusal trauma.
  • Dental impaction.
  • Cysts and tumors.
  • Osteitis.
  • Mucocutaneous diseases.
  • Salivary gland diseases.
  • Atypical facial pain.
  • Glossodynia.

  Aetiology

Disorders

  Dento-alveolar

Dental – dentine sensitivity, cracked tooth, pulpitis

Periodontal – periapical periodontitis, acute necrotizing

ulcerative gingivitis/periodontitis

  Mucosal disease

Ulcerative/erosive disorders including desquamative gingivitis

  Bony pathology

Alveolar osteitis (dry socket)

Osteomyelitis

Infected dental cyst

Osteonecrosis

  Sinusitis

Maxillary, paranasal, ethmoidal and/or frontal

  Salivary glands

Salivary duct calculi causing obstruction

Infective sialadenitis

Salivary gland tumour

  Musculoskeletal

Temporomandibular disorder

  Neuropathic

Trigeminal neuralgia

Glossopharyngeal neuralgia

Trigeminal neuropathic pain and dysaesthesia in relation topathology/iatrogenic nerve damage

Post-herpetic neuralgia

Burning mouth syndrome

  Vascular

Migraine

Tension type headache

Temporal arteritis

TAC (SUNCT/SUNA, PH, CH)

  Other

Chronic idiopathic facial pain

Atypical odontalgia

Central post stroke pain

Cancer – secondaries

  Referred from

 

Eyes

Ears

Intracranial

Heart

  TAC = Trigeminal autonomic cephalalgia

  SUNCT = Short-lasting, Unilateral, Neuralgiform headache with Conjunctival injection and Tearing

  SUNA = Short-lasting, Unilateral, Neuralgiform headache attacks with cranial Autonomic symptoms

  PH = Paroxysmal Hemicrania

  CH = Cluster Headache

  • Cardiac ischemia.
  • Hyperthyroidism.
  • Hyperparathyroidism.
  • Systemic lupus erythematosus.
  • GERD.
  • Diabetes mellitus.
  • Vitamin B deficiencies.
  • Multiple myeloma.
  • Folic acid and iron deficiency anemias.
  • Cancer therapy.
  • Paget’s disease.
  • Metastatic disease.

Neuropathic pain occurs due to a structural abnormality in one or more components of the nervous system that innervate the affected area.

  1. Neuropathic pain may be paroxysmal and continuous disorders.
  2. The most common paroxysmal facial pain is trigeminal neuralgia (TN). Some paroxysmal pains are:
  • Glossopharyngeal neuralgia.
  • Nervusintermedius neuralgia
  • Occipital neuralgia
  • Neuroma
  1. Continuous neuropathic disorders are characterized by constant, unremitting pain of variable intensity. The pain usually has a burning quality and may be accompanied by paresthesia (abnormal sensation) or dysesthesia e.g.:
  • Post-herpetic neuralgia.
  • Post-traumatic neuralgia.
  • Atypical odontalgia.
  1. Periodontal diseases
    • Acute necrotizing ulcerative gingivitis (ANUG).
    • Periodontal abscess.
  2. Recurring oral ulcers
    • Recurrent aphthous stomatitis.
    • Behçet’s syndrome.
    • Recurrent herpes simplex virus infection.
  3. Acute multiple lesions
    • Herpesvirus infections.
    • Primary herpes simplex virus infections.
    • Coxsackievirus infections.
    • Varicella-zoster virus infection.
    • Erythema multiforme.
    • Contact allergic stomatitis.
    • Oral ulcers secondary to cancer chemotherapy.
  4. Chronic multiple lesions
    • Pemphigus.
    • Subepithelial bullous dermatoses.
    • Herpes simplex virus infection in immunosuppressed patients.
  5. Single ulcers
    • Anaerobic infections of oral mucosa.
    • Deep mycoses.
    • Systemic diseases (inflammatory boweldisease)
  • Neck tongue syndrome is characterized by unilateral paroxysmal neck pain in association with ipsilateralparesthesia (numbness)of the tongue.
  • It is triggered by rotation of the neck, usually to the same side as the sensorysigns.

Neuralgia is pain in the distribution of nerve.

The International Headache society has classified neuralgias into two categories according to etiology:

  1. Neuralgias associated with compression of the nerve root or systemic cause, such as multiple sclerosis are considered symptomatic neuralgias.
  2. Neuralgias of unknown cause are called Idiopathic Neuralgias. 

According to theInternational Headache Society (IHS) the trigeminalneuralgia may be defined as “painful unilateralaffliction of the face characterized by brief electricshock like pain limited to the distribution of one or more divisions of trigeminal nerve”.

It is compression of trigeminal nerve root that occurs usually within few millimeters of entering in to the pons. The primary demyelinatingdisorders can also lead to this condition. A few rarecause of trigeminal neuralgia are:

  1. Infiltration of nerve root (due to carcinomatousdeposit within nerve root, gasserian ganglion andnerve )
  2. Small infarcts or angiomas in the pons or medulla.
  3. Infiltration of gasserian ganglion or the nerve by atumour or amyloid.
  1. Vestibular schwannomas.
  2. Meningiomas.
  3. Epidermoid cyst.

It is the typical initial manifestation thatprecedes the classic presentation of TN. A dull continuous, achingpain in the upper or lower jaw that later develop intoclassic paroxysmal pain. This prodromal pain is termedas “pre-trigeminal neuralgia”.

  1. Based on etiology
    1. Classical trigeminal neuralgia – In this, no cause of the symptoms could be identified other than vascularcompression.
    2. Symptomatic trigeminal neuralgia -Has the sameclinical criteria, but other underlying cause isresponsible for the symptoms.
  2. Based on specific, objective, and reproducible criteria: A classification scheme for trigeminal neuralgia (TN) and related facial pain syndromes is proposed. Such a classification scheme is based on information provided in the patient’s history and incorporates seven diagnostic criteria, as follows:
    • 1) and 2) – Trigeminal neuralgia Types 1 and 2(TN1andTN2) refer to idiopathic, spontaneous facialpain that is predominantly episodic (as in TN1) orconstant (as in TN2) as in nature.
    • 3) Trigeminal neuropathic pain results from unintentional injury to the trigeminal nerve from trauma or surgery.
    • 4) Trigeminal differentiation pain results from intentional injury to the nerve by peripheral nerve ablation, gangliolysis or rhizotomy in attempt to treat either TN or other related facial pain.
    • 5) Symptomatic TN results from multiple sclerosis.
    • 6) Post-herpetic TN follows a cutaneous herpes zoster outbreak in the trigeminal distribution.
    • 7) The category of atypical facial pain is reversed for facial pain secondary to somatoform pain disorder and requires psychological testing for diagnostic confirmation.
  3. Based on symptoms
  4. From symptomatic point of view the trigeminalneuralgia is classified in to following:
    1. Typical Trigeminal Neuralgia (Tic Douloureux)
    2. This is the most common form of TN, which haspreviously been termed Classical, Idiopathic andEssential TN.
    3. Atypical trigeminal neuralgia
    4. Atypical TN is characterized by a unilateral, prominentconstant and severe aching, boring or burning painsuperimposed upon otherwise typical TN symptoms.
  • Recurring episodes of intense, short-lived spasmsof pain of the lower portion of the face and jaw.
  • Pain is limited to one side of theface (unilateral).
  • The pain has been compared to a series of”electrical shocks” followed by a steady dull ache.
  • The pain often starts and stops rapidly.
  • Intense pain usually lessens rapidly (usually withinseveral seconds), but the following dull achingpain may persist for as much as one to twominutes.
  • Sensitivity in certain areas of facecalled trigger zone, which when touched cause anattack.These zones are usually near the nose, lips,eyes, ears or inside the mouth.
  • Pain may be triggered by mild tactile stimuliincluding brushing one’s teeth, washing one’sface, shaving, drinking hot or cold drinks,chewing, talking, blowing one’s nose, a coolbreeze, or a light touch to the face.
  • Some episodes may occur without an apparenttrigger (spontaneously). Consequently, episodescan occur repeatedly throughout the day.
  • Episodes rarely occur during sleep.
  • Attacks typically stop for a period of time and thenreturn.
  • Over the time, the pain tends to grow worse withfewer pain-free periods.
The diagnostic criteria of the International HeadacheSociety (IHS) (1988) are as follows:
  1. Paroxysmal attacks of facial pain that lasts a fewseconds to less than two minutes.
  2. Pain has at least 4 of the following characteristics:
    1. Distribution along one or more divisions ofthe trigeminal nerve.
    2. Sudden, intense, sharp, superficial, stabbing orburning in quality.
    3. Pain intensity is severe.
    4. Precipitation from trigger areas, or by certainactivities such as eating, talking, washing theteeth or cleaning the face.
    5. Between paroxysms the patient is entirelyasymptomatic.
  3. Attacks are stereotyped in the individual patient.
  4. No neurological deficit and exclusion of othercauses.
In the second edition the diagnostic criteria forclassical trigeminal neuralgia are as follows:
  1. Paroxysmal attacks of pain lasting from fraction ofa second to two minutes, affecting one or more divisionof trigeminal nerve and fulfilling criteria B&C.
  2. Pain has at least one of the following characteristics:
  • Intense, sharp, superficial or stabbing.
  • Precipitated from trigger area or by trigger factor.
  1. Attacks are stereotype in the individual patients.
  2. There is no clinically evident neurological defect.
  3. Not attributed to another disorder.
The trigeminal neuralgia association, UK has given thefollowing clues that point to a correct diagnosis:
  1. The degree of pain exceeds the evidence.
  2. Painkillers do not kill the pain.
  3. The pain cannot be pinned down to one specifictooth
  4. Radiologic investigations are important. Secondary TN (e.g. multiple sclerosis, cysts,vascular pathologies etc.) can be ruled out with help ofMRI.
  1. Autonomic signs & SUNCT:
  • “Short lasting unilateral neuralgiform headache attacks with conjunctival injection & tearing”.
  • Brief unilateral pain attacks (5- 240 sec in duration) in the orbital area.
  • Facial redness, conjunctival injection, lacrimation, & nasal congestion/ rhinnorrhea.
  • These involve the mid-face & orbital region.
  1. Cluster- tic syndrome:

Cluster headache together with TN

(Cluster headache is a well defined craniocervical pain syndrome characterized by episodes of severe unilateral pain in the orbital region lasting 15- 180 min. repeated pain episodes occur in “clusters”)

  1. Hemifacial spasm, tic convulsif, & TN
  • Hemifacial spasm or tic convulsif is a disorder characterized by intermittent contractions of the muscles of facial expression on one side
  • Spontaneous twitch contraction (tics) are common.
  • Results from chronic, mild compression injury of the facial nerve.

Differential diagnosis includes: Migraine, Sinusitis, Post herpetic neuralgia, Trigeminal neuritis or trigeminal neuropathy, Pain of dental origin, Trotter’s syndrome.

Pharmacological management can be divided in to:

  • First line: Carbamazepine or oxcarbazepine
  • Second line: Baclofen or lamotrigine
  • Third line: Levetiracetam, gabapentin, pregabalin, topiramate, Botox-A
  1. Drug– Carbamazepine

Mechanism of action: Slow the recovery rate of voltage sensitive sodium channels, modulates activated calcium channel activity and activates descending inhibitory modulation system

Dose: 200-1200 mg daily in 2 divided doses

Adverse effect:Memory problems, diplopia, drowsiness, fatigue, nausea, nystagmus liver dysfunction,hematosupression

  1. Drug – Baclofen

Mechanism of action: It is GABA analogue that activates GABAB receptors and thus depresses excitatory neurotransmission.

Dose: Initial dose is 5mg TID for3 days and dose may beincreased up to10 to 20mg/day every 3 days andmaximum tolerated dose is50 to 60 mg/day

Adverse effects– drowsiness, dizziness,weakness, fatigue andnausea.

  1. Drug – Oxcarbazepine

Mechanism of action: Act by blocking voltage sensitive sodium channel and it modulates voltage activated Ca++ currents.

Dose: 300 to 1800 mg daily intwo divided doses

Adverse effect – Dizziness, fatigue, ataxia,fatigue, tremors, diplopia,diminished concentration.

  1. Drug – Phenytoin

Mechanism of action: Promotes sodium reflux from neurons.

Dose: 300 to 500 mg/day

Adverse effects: Nystagmus, ataxia, slurredspeech, mentalconfusion.

  1. Drug – Lamotrigine

Mechanism of action:It acts as a voltage sensitive sodium channel and stabilizes neural membranes

Dose: Starting dose is 25 mg twice daily and it can beincreasedgradually to a maintenancedose of 200-400mg/day intwo divided doses.

Adverse effect – Ataxia, constipation, vomiting and rash.

  1. Drug – Levetiracetam

Mechanism of action:Mechanism of action is thought toinvolve binding to the high voltage N type calcium channelsas well as the synaptic vesicleprotein 2A (SV2A).

Dose: Effective dose range is1000 – 4000mg/day

Adverse effect – Sleepiness, fatigue,weakness, headache, pain,double vision, dizziness,coordination difficulties,runny nose or cough,increased infections,

memory difficulties,anxiety, and behavioralproblems

7.Drug – Gabapentin

Mechanism of action– It is GABA receptor agonist, acts primarily on presynaptic calcium channels of neurons to inhibit the release of excitatory neurotransmitters.

Dose – 900 to 1800 mg daily in3 or 4 divided doses

Adverse effect – Dizziness, coordination problems, nausea, vomiting.

  1. Drug– Pregabalin

Mechanism of action – Drug binds to the alpha-2-delta  subunit of the voltage gated calcium channels causing decreased presynapticcalcium entry leading to decreased synaptic release of glutamate.

Dose – 150-600 mg/day.

Adverse effect- Ataxia.

  1. Drug– Topiramate.

Mechanism of action – Acts by sodium channel blockade enhancing GABAA activity by binding to a non-benzodiazepine site on GABAA receptors, and selectively blocking AMPA/kainiteglutamate receptors.

Dose– 100 to 400 mg a day

Adverse effect– Dizziness, sedation, cognitive impairment, fatigue, nausea, blurred vision and weight loss.

If there is failure of at least 3 drug trials, or drugs are causing unacceptable side effects, and according to the candidate’s medical status, age, or preference.

    1. Microvascular decompression
    • This permits the trigeminal nerve nucleus to recover from its state of hyperactivity and return to a normal, pain free condition.
    • Micro-instruments are used to mobilize the offending vessels away from the trigeminal nerve root.
    • The decompression is permanently maintained by inert implants, such as those made of shredded Teflon®, between the offending vessels and nerve.
    1. Percutaneous Rhizotomies

    Involve inserting a needle through the cheek and into an opening at skull base (foramen ovale). There, a controlled injury to the trigeminal nerve and Gasserion ganglion may be produced in one of three ways:

    • Percutaneous Glycerol Injection.
    • Percutaneous Balloon Compression Rhizotomy.
    • Radiofrequency Rhizotomy.
    1. Gamma Knife Radiosurgery

    Focuses cobalt radiation upon the trigeminal nerve root, producing a delayed injury to nervous tissue.

    1. Peripheral Trigeminal Nerve Blocks, Sectioning and Avulsions

    Involve injuring the peripheral portions of the trigeminal nerve external to the skull.

    1. Microsurgical Rhizotomy

    Involves surgical exposure and cutting of the trigeminal nerve root near its entry into the brain stem.

Uncommon paroxysmal neuralgia of cranial nerve VII.

  • Characterized by pain in ear, less frequently the anterior tongue and soft palate.
  • Location of pain – external auditory canal, a small area on the soft palate and posterior auricular region
  • Pain provoked by stimulation of trigger zones within the ipsilateral distribution of nerve
  • Pain is not as sharp or intense as trigeminal neuralgia
  • Facial paralysis due to simultaneous involvement of motor root.

HZ of the geniculate ganglion, Ramsay Hunt syndrome, isa rare form of the disease characterized by Bell’s palsy, unilateralvesicles of the external ear, and vesicles of the oral mucosa.

  • Short course (2 to 3 weeks) of high dose steroid therapy is beneficial.
  • Acyclovir 800 mg 5 times/ day for 10-14 days – decreases pain.
  • Can be treated with Carbamazepine and Antidepressants.
  • Patients who do not respond to these medication may undergo surgery to section the nervusintermedius.

Post herpetic neuralgia, trigeminal neuritis or trigeminal neuropathy, pain of dental origin.

The International Association for theStudy of Pain (IASP) defines it as sudden, severe, brief, recurrentpain in the anatomical distribution of theglossopharyngealnerve.

  • Trigger zone: Pharynx, Posterior tongue, ear.
  • Pain triggered by chewing, talking and swallowing, all of which stimulate the pharyngeal mucosa.
  • No gender predilection.
  • Middle age or older person.
  • Sharp shooting pain in ear, pharynx, nasopharynx, tonsil or the posterior portion of tongue.
  • It is invariably unilateral.
  • May be associated with vagal symptoms – syncope and arrhythmia.
  • Intracranial or extracranialtumors and vascular abnormalities that compress cranial nerve 9th.
  • Neural ischemia.
  1. According to Anatomical Area Involved:
    • Otitic type – Pain in and around the ear.
    • Oropharyngeal – Pain is in and around throat and face region.
  2. The types proposed by International Headache Society(IHS) are:
    • Classical GPN– episodic pain
    • Symptomatic GPN– continuous pain, commoner.
  3. Cause-based Classification
    • Idiopathic type: No demonstrable lesion is found in these cases.
    • Secondary type (Symptomatic): In this, a demonstrable lesion can be found like trauma, neoplasm, infection, vascular malformation, or elongated styloid process.
  • The diagnosis of GPN is strictly clinical.
  • In any pain with typical glossopharyngeal distribution, ascertainits predominant distribution: Tympanic or oropharyngeal.
  • Check if the trigger point is in the oropharyngeal area or is in theEar.
  • Is the neuralgic pain precipitated orally or it is brought about by hearing activities e.g. pain on exposure to loud sounds.
  • If the patient does not have pain at that point of time, but anticipates that he would have it later in the day, the triggerpoint may be injected with lignocaine 2% or bupivacaine 0.5% to see if it can avert another attack of pain. If the symptomsare primarily otologic, inject lignocaine 2% or bupivacaine0.5% into the external auditory meatus to see if it abolishes thepain that is present at that time or it will avert a subsequentattack. 

Investigations

Laboratory test:

Complete blood count, Erythrocyte sedimentation rate, Anti-nuclear antibody, automated serum chemistry to rule out occult systemicdiseases like temporal arteritis, infection, inflammation, andmalignancy.

Imaging of the brain includes:

  • Non-contrast MRI
  • Magnetic resonance angiography (MRA)
  • 3-dimensional computed tomography angiography (3D-CTA)- To rule out nerve compression by a vessel or any tumor or by any other bony structure or signs of demyelination.

The International Association for the Study of Pain (IASP) recommended drugswith their dosages usedin GN:

  Drug

Dose mg/day

  Carbamazepine

100-2000

  Gabapentin

900-1800

Duloxetine        

20-90

Valproicacid   

125-2500

Clonazepam

0.5-8

Lamotrigine

50-500

Baclofen

10-80

Phenytoin

200-600

Pregabalin

75-500

Topiramate

50-1000

Glossopharyngeal nerve blocks- They can be performed witheither non-neurolytic agents (local anesthetic agents) with orwithout additives (steroid, ketamine, etc.) or with neurolyticagents (phenol, alcohol, glycerol, etc.)

Surgical procedures for the lesions may be classified as follows:

Peripheral procedures:

  • Extra cranial, such as direct surgical neurotomies orpercutaneous radiofrequency thermal rhizotomy.
  • Intracranial, such as direct section of glossopharyngealand vagal nerves in the cerebello-pontine angle.
  • Central procedures, such as percutaneous or opentrigeminal tractotomy-nucleotomy or nucleus caudalis DREZ (dorsal root entry zone) operation

Superior laryngeal neuralgia was first described asa painful laryngeal pressure point by Tobold (1866).

  • It is a rare disorder.
  • Pain paroxysms, lasting for minutes or hours, triggered by swallowing, straining the voice, or head turning.
  • A trigger point is present on the lateral aspect of the throat overlying the thyrohyoid membrane. 

The etiology is still unclear. Predisposing factors are:

  • A minor upper respiratory tract disease
  • Influenza.
  • Laryngitis
  • After microsurgery or trauma.
  • Previous tonsillectomy
  • Lateral pharyngeal diverticulum.
  • Compression of the nerve by the superior thyroid artery and/or vein.
  • Viralinfection may cause neuropathy by direct infection or inflammation of the nerve or by a nonspecific inflammatory response that secondarily involves a nerve.
  • Electromyography to verify the function of the various laryngeal muscles.
  • Computed tomographic scanning of the larynx for any pathologic conditions in laryngeal and peri-laryngeal structures.
  • Endoscopic examination showed hyperemia and edema of the vocal folds

Pharmacological

  • Carbamazepine- 100-2000mg/day.
  • Gabapentin- 900- 2400mg/day.

Surgical

  • Intracranial section of the upper vagal rootlets.
  • Percutaneous thermal rhizotomy.
  • Extracranial section of the superior laryngeal nerve.

According to International Headache Soci­ety (IHS), occipital neuralgia (ON), also known as C2 neuralgia, involves paroxysmal shooting or stabbing pain in the derma­tomes of the greater occipital nerve (GON or nervusoccipitalis major) and the lesser occipital nerve (LON or nervusoccipitalis minor).

Vascular

  • Irritation of the C1/C2 nerve roots by an aberrant branch of the posterior inferior cerebellar artery.
  • Dural arteriovenous fistula at the cervical level.
  • Bleeding from a bulbocervicalcavernomas.
  • Cervical intramedullar cavernous hemangioma.
  • Giant cell arteritis.
  • Fenestrated vertebra artery pressing on C1/C2 nerve roots.
  • Aberrant course of the vertebra artery.

 

 

Neurogenic

  • Schwannoma in the area of the craniocervical junction: schwan­noma of occipital nerve.
  • C2 myelitis.
  • Multiple sclerosis.

Osteogenic

  • C1/C2 arthrosis, atlantodental sclerosis
  • Hypermobile C1 posterior arch
  • Cervical osteochondroma.
  • Osteolytic lesion of the cranium.
  • Exuberant callus formation after C1/C2 fracture.
  • Shooting or stabbing pain in the neck that radiates over the cranium.
  • Pain is characterized as persistent, paroxysmally aggravating, and of variable distri­bution; can be perceived in the retro-orbital area due to the con­vergence of the C2 dorsal root and the nucleus trigeminus pars caudalis.
  • Due to connections with the VIII, IX, and X cranial nerves and the cervical sympathicus, vision impairment/ocular pain, tinnitus, dizziness, nausea and congested nose can also be present.
  • Hypoesthesia or dysesthesia can occur.
  • The pain is located in the occipital area and may spread toward the vertex.
  • Pain is usually unilateral.

The diagnostic criteria are:

  • Paroxysmal stabbing pain, with or without persistent aching between paroxysms, in the distribution of the greater, lesser, and/or third occipital nerve.
  • Tenderness over the affected nerve.
  • Pain is eased temporarily by local anesthetic block of the nerve.
  • Along GON (over the occipital protuberance) and/or the LON (about 3 cm superomedially to the tip of the mastoid process), tenderness is detected by palpation.
  • Tin­gling may be evoked by light pressure or percussion on the nerve which is known as Tinel’s sign.
  • When patients lie on a pillow and hyperextend or rotate their neck, pain can occur that is known as Pillow sign.
  • Temporary improvement in headache with a lo­cal anesthetic diagnostic block of the occipital nerve on the af­fected side confirms the diagnosis.

Imaging studies

  • Magnetic resonance imaging- Visualization of the sur­rounding cervical and occipital soft tissues.
  • Simple X-ray- for underlying pathologies, such as arthritis and craniocervical instability.
  • CT scan of the craniocervical junc­tion can reveal neoplastic or degenerative osseous pathology.

Migraine, cluster headache, tension headache or hemicra­nia continua.

Conservative treatment:

  • Posture correction and reduc­ing the neuralgic and muscle pain.
  • Pharmacological treatment may include tricyclic antidepressants, serotonin reuptake in­hibitors, anticonvulsants (e.g., carbamazepine, oxycarbamaze­pine, gabapentin, pregabalin), and opioids.

Interventional management

  • Local anesthetic agent injection with or without steroid.
  • Botulinum toxin infiltrations.
  • Pulsed radiofrequency treatment.

Surgical treatment:

  • Neurolysis
  • Occipital nerve stimulation

According to the International Association for the Study of Pain Postherpetic neuralgia can be defined as “chronic pain following resolution of acute herpes zoster that is accompanied with skin degeneration in the affected dermatome.”

Chen N et al gave the distinction between acute herpetic neuralgia (within 30 days of rash onset), subacute herpetic neuralgia (30 to 120 days after rash onset), and PHN (defined as pain lasting at least 120 days from rash onset).

Patients with PHN experience three major types of pain:

  • Constant pain without a stimulus (often described as burning, aching, or throbbing).
  • Intermittent pain without a stimulus (often described as stabbing, shooting, or electric shock-like).
  • Pain brought on by a stimulus but is disproportionate to the stimulus (hyperalgesia) enduring for at least 3 months after healing of the HZ-related skin rash. In addition, patients may experience a variety of abnormal sensations (dysesthesias or paresthesias)

  Topical agents

Lidocaine: 5% patch; apply up to 3 patches at a time to affected area; use up to 12 h in a 24-h period Capsaicin: 0.075% cream; apply at least 3 times daily

  Antidepressants TCAs

Nortriptyline/amitriptyline: start at 10-20 mg/d; increase dose in 10 mg increments every 3 to 5 d until satisfactory pain relief is achieved or intolerable adverse effects occur, to maximum of 100 mg/d

  SNRI = selective serotonin and                  norepinephrine reuptake inhibitor

Venlafaxine:start at 37.5 mg/d increase dosage to a maximum of 225 mg/d

 Duloxetine: start at 20 mg at bedtime; increase by 20 mg every 5 d to a maximum of 60 mg/d.

  Anticonvulsants

Gabapentin: 300 mg on day 1

300 mg twice daily on day 2, and

300 mg 3 times daily on day 3

may increase dosage up to 1800 mg/d (divided in 3 doses)

Pregabalin: 75 mg/d at bedtime; increase by 75 mg every 5 d to maximum of 300 mg twice daily

  Opioids

Oxycodone: 5 mg every 4-6 h; increase by 5- to 10-mg increments as needed to 40 mg/d

Tramadol: start at 25 mg twice daily; increase every 3 d to a maximum of 200 mg/d

A sinus infection can create pressure and pain in the mouth and cause a sinus tooth pain. Sinus tooth pain is often confused with other causes of tooth pain, including gum disease, tooth decay, or an impacted wisdom tooth.

  • Posterior maxillary teeth most commonly involved.
  • Teeth will respond to vital pulp testing and will not exhibit thermal sensitivity.
  • Pain varies with changes in head position is suggestive of sinusitis.
  • Facial symptoms may include unilateral paresthesia, anaesthesia, and midface fullness.
  • There may be change in vision, diplopia, altered eyeball position, and epiphora.
  • Nasal symptoms may include epistaxis, allergic rhinitis and postnasal drip.
  • Intra-orally, tooth pain and sensitivity, paresthesia or anaesthesia of the gingiva and mucosa as well as a feeling of alveolar expansion or malocclusion may be experienced.
  • History of previous episodes of sinusitis.
  • Clinical exam; palpation of maxillary bone over the sinuses and evaluation of the teeth to identify a possible dental origin.
  • Radiographs, including periapical and possibly panoramic x-rays.
  • Vitality testing of the tooth, including electric pulp testing, ice, heat, and percussion
  • Rule out sinusitis by treating the pain with a drug regime effective in treating sinusitis.
  • Panoramic radiograph depicts both maxillary sinuses, revealing greater internal structure and parts of the inferior, posterior, and anteromedial walls.
  • The occipitomental (Waters), lateral, submentovertex and Caldwell (150 PA) skull views.
  • TheWaters projection is optimal for visualization of maxilliary sinuses, especially to compare internalradio-opacities, as well as the frontal sinuses and ethmoidair cells.
  • If the Waters view is made with the mouthopen, the sphenoid sinuses may also be visualized.

Also known as Sphenopalatine ganglion neuralgia, lower-half headache, Sluder’s headache, vidian nerve neuralgia, atypical facial neuralgia, histamine cephalgia, Horton’s syndrome, Sphenopalatine Neuralgia, periodic migrainous neuralgia

Cluster headache (CH) is a unilateralheadache that occurs inassociation with cranial autonomicfeatures.

The term cluster is used because the individual experienced multiple headaches per day for 4 to 6 weeks and then may be without pain for months or even years.

  • Episodic: Occurs in periods lasting 7 days to 1 year separated by pain-freeperiods lasting 1 month or more
  • Chronic: Attacks occur for more than 1 year without remission or with remissionslasting less than 1 month

Headache must have each of:

    • Severe, unilateral, orbital, supraorbital and/or temporal pain lasting 15-180

minutes untreated.

  • Frequency of attacks: from 1 every other day to 8 per day.
  • Headache associated with at least 1 of the following signs that have to be present on the pain side:
  • Conjunctivalinjection.
  •  Lacrimation.
  • Nasal congestion.
  • Rhinorrhoea.
  • Forehead and facial sweating.
  • Miosis.
  • Ptosis.
  • Eyelid oedema
  • Sense of restlessness or agitation during headache.

Migraine, paroxysmal hemicrania, SUNCT syndrome, hemicrania continua, hypnic headache.

  • Good clinical history and a detailed neurologicalexamination.
  • A magnetic resonanceimaging (MRI) scan of the brainis a reasonable screening investigation.
  1. Good efficacy:
    • Oxygen 100 per cent at 7-12 litres per min for15-30 minutes.
    • Sumatriptan subcutaneous injection 6mg(maximum twice daily for the duration of thecluster bout)
  2. Moderate efficacy:
    • Sumatriptan nasal spray 20mg (maximum 3times daily for the duration of the cluster bout).
    • Octreotide subcutaneous injection 100mg.
    • Zolmitriptan5 or 10mg (for episodic clusterheadache only)
  3. Poor efficacy or unproven
    • Ergotamine tablets or suppository
    • Intranasal lidocaine

Carotidynia is defined as unilateral neck pain sometimes radiating to the ear, teeth, mandible and eye. The only physical sign is tenderness onpalpation of the carotid artery.

  • The term ‘carotidynia’ was initially described by Fay in 1927.
  • It was classified by the International Headache Society (IHS) in 1988 as an idiopathic neck pain syndrome associated with tenderness over the carotid bifurcation without structural abnormality.
  • The aetiology is not known but it has been proposedto be a subset of vasculitis.
  • Inflammation in or around the carotid artery wall.
In 1988, acute idiopathic carotidynia was classifiedby the International Headache Society (IHS) ClassificationCommittee based on four diagnostic criteria:
  1. At least one of the following overlying the carotid artery:
    1. Tenderness.
    2. Swelling.
    3. Increased pulsations.
  2. Appropriate investigationsdo not reveal structural abnormality.
  3. Pain over the affectedside of the neck,may project to the ipsilateral side of the head.
  4. A self-limiting syndrome of less than 2-weeks duration.
  • CT OR MRI to rule out carotid body tumor or carotid aneurysm.
  • Ultra-sonography of the carotidartery.
  • Elevated C-reactive protein (CRP).
  • Elevated erythrocyte sedimentation rapidity (ESR).
  • Elevated Serum amyloid A (SAA) protein.
  • Idiopathic form – self limited in 1 to 2 weeks
  • Anti-inflammatory drugs and steroids are the drugs of choice and are highly effective.

This category includes pain syndromes considered by IASP as generalised conditions.

  • Peripheral neuropathy or Radiculopathy.
  • Causalgia and reflex dystrophy.
  • Central pain.
  • Stump pain.
  • Phantom pain.
  • Pain of purely psychologic origin.

Peripheral neuropathy may be defined as constant or intermittent burning, aching, or lancinating limb pains due to generalized or focal diseases of peripheral nerves.

Peripheral neuropathy occurs due to nerve fiber damage, usually axonal degeneration. Pain especially occurs with small fiber damage (sensory fibers).

It involves usually distal (especially the feet) with burning pain, but often more proximal and deep with aching.

  • Common in neuropathies of diabetes, amyloid, alcoholism, polyarteritis, Guillain-Barre Syndrome, neuralgic amyotrophy, Fabry’s disease.
  • Usually occurs after second decade.

Pain Quality:

    1. Burning, superficial, distal pain often with dysesthesia, constant. May be in

the territory of a single affected nerve.

  1. Deep aching, especially nocturnal, constant;
  2. Sharp lancinating “tabetic” pains (back pain/lightning limb pain), especially in legs, intermittent.

Associated Symptoms:

Sometimes patient may also feel:

  • Sensory loss, especially to pinprick and temperature.
  • Weakness and muscle atrophy (especially in neuralgic amyotrophy).
  • Reflex loss
  • Signs of loss of sympathetic function
  • Smooth, fine skin
  • Hair loss.
  • Features of the primary disease, e.g., diabetes
  • Features of neuropathy: reduced or absent sensory potentials, slowing of motor and sensory conduction velocities, EMG evidence of muscle denervation.

Pain at the site of an extremity amputation.

Neuroma at the site of nerve transection.

  • Pain usually occurs in upper or lower extremity at the region of amputation.
  • Pain is not referred to the absent body part but is perceived in the stump itself, usually in region of transected nerve(s).
  • Sharp, often jabbing pain in stump, usually aggravated by pressure on, or infection in, the stump.
  • Pain often elicited by tapping over neuroma in transected nerve or nerves.
  • Refusal to utilize prosthesis.
  • Pain elicited by percussion over stump neuromata.
  • Alter prosthesis to avoid pressure on neuromata.
  • Resect neuromata so that they no longer lie in pressure areas;
  • Utilize neurosurgical procedures such as rhizotomy and ganglionectomy or spinal cord or peripheral nerve stimulation in properly selected patients.

Pain referred to a surgically removed limb or portion thereof.

Occurs in the absent body part.

Phantom pain is believed to be more common if loss of limb occurs later in life, in limbs than in breast amputation, in the breast before the menopause rather than after it, and particularly if pain was present before the part was lost.

  • Pain may be continuous, often with intermittent exacerbations, usually cramping, aching, burning; mayhave superimposed shocklike components.
  • Seems to be less likely if the initial amputation is treatedactively and a prosthesis is promptly utilized.
  • Phantom limb pain is almost always associated withdistorted image of lost part.
  • No therapeutic regimen has more than a 30% long-term efficacy.
  • TENS, anticonvulsants, antidepressants, or phenothiazines may be helpful.
  • Sympathectomy or surgical procedures upon spinal cord and brain, including stimulation, are sometimes helpful.

Also known as Complex Regional Pain Syndrome,Causalgia.

Reflex-sympathetic dystrophy is characterized by unpleasant persistent burning pain accompanied by sympathetic disorder and progressive trophic changes leads to:

  • Decrease blood flow.
  • Perspiration abnormalities.
  • Muscle atrophy.
  • Regressive changes of skin and bones.

Development of RSD requires the following triad of conditions:

  • An injury.
  • An abnormal sympathetic response.
  • A predisposing personality.
  • The pain in RSD occurs as the sympathetic reflex, begins to feedback and set off a viscious cycle of pain. The sustained sympathetic excitation due to painstimulation induces peripheral vasoconstriction with resultant regional circulatory disturbances, which inturn stimulate nociceptors to accelerate the pain.
  • Rare in orofacial region due to decreased number of sympathetic neurons identified in branches of trigeminal nerve as compared to number found in nerves of upper extremity.

They are two types:

  • Sympathetically maintained pain (SMP)
  • Sympathetically independent pain

It is divided in 3 stages:

  • Acute
  • Dystrophic
  • Atrophic
  • Burning and aching (sympathetic denervation or underactivity).
  • Increased blood flow to the affected area.
  • Concomitant rise in skin temperature.
  • Edema; dependent rubor; decreased heat intolerance.
  • X-ray may reveal bony changes in affected areas.
  • Pain becomes constant
  • Parodoxic, sympathetic overactivity; cold intolerance; hyperaesthetic pain
  • Blood flow decrease in area
  • Decrease in skin temperature
  • Early signs of subcutaneous atrophy and patchy osteoporosis.
  • Pain diminishes in intensity and tends to spread proximally with continued atrophy and tissue damage.
  • Skin appears smooth, glossy, muscle wasting & concomitant loss of strength become overt.
  • Tendon contractures with decreased range of motion.
  • Radiographs disclose marked demineralization.
  • Associated with wide range of behavioral and emotional changes.
  • Bone scan.
  • Doppler studies.
  • Plethysmography.
  • Thermography.
  • Phentolamine test.
  • Series of diagnostic and therapeutic stellate ganglion blocks with lignocaine.
  • If initially a positive response – injections continued till improvement 3-6 stellate ganglion blocks over 2 to 12 weeks period produce long lasting improvement.
  • Physical therapeutic modalities with TENS.
  • Topical prostaglandin E1 ointment can be effective. 
  • Also known as atypical facial neuralgia, facial causalgia.
  • It refers to pain that does not conform to recognized anatomic pathways in its distribution. 
  • It cannot be relieved by interruption of trigeminal or glossopharyngeal pathways.
  • It has no identifiable neuropathic or non neuropathic (extraneural or central) focus.
  • It is associated with a potential pain producing focus but that is out of proportion to the focus or not strictly related to its terms of recognized anatomic pathways and physiological mechanism.
  • It is called as “GRAB-BAG CATEGORY” Or Syndrome with multiple etiologies.
  • Role of peripheral trauma leading to chronic neuropathic pain.
  • Chronic pain for any causes.
  • Psychological behavior.
  • Necrotizing intrabony cavitational osteonecrosis.
  • Patient’s inability to define a precise location and quality of pain.
  • Gives deep dull ache history.
  • Gives discursive & wandering replies during taking history.
  • Complains of burning,dryness and taste aberrations
  • Pain described is worst pain he/she ever had.
  • Emotional breakdown, tear, hysteria.
  • History of crying or frustration due to chronic pain.
  • Patient appears sad, unhappy face and an inability to respond in a positive, happy way to any question.
  • Depression of some degree to accompany all chronic pain.
  • Frequently middle aged.
  • Female: male = 19:1.
  • Long history of chronic facial pain or dysesthesia.
  • Usually unilateral initially, later bilateral symptoms
  • Poorly defined quality & location of pain
  • Patientwith long history of successive, unsuccessful surgical or medical treatments with progressive worsening of the complaint.
  • Patient do not exhibit altered somatosensory thresholds
  • Patient should be recalled for further evaluation at regular interval if diagnosis of atypical facial pain is made.

MPDS & TMJdisease, Pain of vascular origin,Trigeminal neuralgia, Eagles syndrome, Atypicaltrigeminal neuralgia, Odontogenic pain, Neuropathy

  • Medical treatment is less satisfactory
  • Tricyclic antidepressants (amitryptyline, nortryptyline) give best results. They appear to block re-uptake of norepinephrine & serotonin, transmitters released by pain modulating system in the spinal cord & brainstem, thereby allowing long periods of diminished neural activity.
  • The dose is slowly increased from 25 mg nocte (every night) for the first week, to 50 mgnocte for the second week, and then to 75 mg nocte for the third and ensuing weeks, tobuild up patient tolerance to side effects such as sedation. For the elderly, it is prudent tocommence with a dose of 10 mg nocte for the first week. It is necessary to maintain thetricyclic for at least 12-18 months before considering the discontinuation of the drug.
  • Topical capsaicin in case of localised area involvement.
  • Phenytoin is of intermediate effect.
  • Psychotherapy, behaviour modification, TENS & sympathetic nerve blocks are also helpful.

It isalsoknown as Idiopathic odontalgia ; periodontalgia; phantom tooth pain. Atypical Odontalgia has been described by Merskeyas “Severethrobbing pain in the tooth without major pathology.”Atypical odontalgia can have both psychological and neuropathic origin.

  • It is a condition of persistant pain in the teeth, face or alveolar process that follows pulp extirpation, apicoectomy, or tooth extraction.
  • Molar and premolars are more frequently involved, and the maxilla is more often affected than themandible.
  • Incidence- 3-4% of endodontic treated patients.
  • Well localized character of pain.
  • Age distribution- middle age.
  • Female predominance.
  • Patient complains of constant, dull, deep aching pain with occasional spontaneous sharp pain; no refractory period.
  • It is atypical; psychologic  or somatoform  facial pain.

There are following diagnostic criteria for atypical odontalgia:

  1. Proposed Diagnostic Criteria of Marbach
  • The onset of pain is usually associated with an injury to a peripheral nerve. The injury often occurs in the course of routine dental and medical surgical procedures. Injuries also occur as the result of physical trauma to the face.
  • The onset of the pain does not necessarily coincide with differentiation (pain that results from complete or partial interruption of afferent nerve impulses) at the tooth site. Pain may be delayed for days, weeks, months, or perhaps years.
  • The pain may endure long after healing of the injured tissues and spread to the adjacent healthy tissue. Spreading can follow synaptic reorganization of an injured afferent nerve with resulting structural and functional changes in associated areas.
  • PTP (phantom tooth pain) is more likely to develop in patients who have suffered pain in the tooth or face in the period immediately before the peripheral nerve section or endodontic treatment.
  • The pain is described as constant, dull, deep ache with occasional spontaneous sharp pains. There are no refractory periods.
  • Sleep is undisturbed by pain. Many cases report a brief pain-free period upon awakening. This period lasts from seconds to about 1 hour.
  • Peripheral stimuli can momentarily exacerbate the pain but have no prolonged influence. Percussion over the site of the injured nerve may result in Tinel’s sign (sensation of tingling or ‘pins and needles’ in the distribution of the nerve).
  • These stimuli can be of a type normally non-nociceptive. There appears to be a lowered pain threshold (allodynia).
  • The pain is often worse at the site of the original trauma; although in chronic cases patients have difficulty in localizing the pain, which is in part the result of pain spreading to the adjacent tissues. Additionally, precise localization of tooth pain is difficult. The treatment of neighboring teeth obscures the original condition. Non-painful phantom phenomena also confound accurate perception and localization of the pain site.
  • Radiographic and laboratory tests are negative.
  • Without early intervention, the pain is often permanent once it is established.
  • PTP occurs in both sexes.
  • PTP has been reported in adults but not in children.
  • There is no evidence currently that PTP is characterized by a premorbid personality. Whether affective states such as major depression are a cause or a consequence of chronic pain remains to be determined.
  1. Revised Criteria of Marbach:
  • Pain is located in the face or described as a toothache.
  • The pain is described as a constant dull, deep ache. (Less than 10% of sufferers report occasional spontaneous sharp pains that overlay the ache. Sharp pain is not essential to meet criteria.)
  • A brief (seconds to minutes) pain-free period is reported upon awakening from sleep. There are no other refractory periods.
  • Pain develops (or continues) within one month following endodontictreatment or tooth extraction, or other trauma or medical procedure related to the face.
  • Overlying the area of dental (or other) treatment (usually on the surface of the face but occasionally intraorally) is a location with a much lowered pain threshold (hyperalgesia), often surrounded by a larger area with less severe hyperalgesia.
  • Sleep is undisturbed by pain or other phantom sensations.
  • No radiographic or laboratory tests suggest other sources of pain.
  1. Atypical Odontalgia: Proposed Diagnostic Criteria of Pertes et al
  • Aching, burning or throbbing.
  • Moderate intensity.
  • Continuous or almost continuous pain.
  • No obvious local cause.
  • Normal radiographs.
  • Pain present more than 4 months.
  • Increased sensitivity to pressure.
  • Somatic block equivocal.
  • Non-responsive to analgesics, surgery and dental procedures.
  1. Imaging.
  2. Biopsies.
  3. Human blink reflex (BR)– Several studies have found that patients with AO had altered responses bilaterally when compared to healthy
  4. Thermography- Thermography is a technique of measurement of skin temperature distribution on the body over a given period of time. Patients with AO presented with either hot or cold thermograms on the affected side.
  5. Quantitative sensory testing (QST) – QST is the assessment of the sensitivity to mechanical, thermal, chemical and electrical stimuli with the use of a battery of tools specially designed for this purpose.

Pulpal toothache, trigeminal neuralgia, temporomandibular joint disorders, myofascial pain, pretrigeminal neuralgia, sinusitis, ear and eye problems, cracked tooth syndrome.

  1. Topical anesthetic – Mixture of lidocaine and prilocaine (Eutectic mixture of local anesthetics-EMLA 6% lidocaine + prilocaine)
  2. Tricyclic antidepressants (TCAs):
    • Amitriptyline is most commonly used.
    • Doses starts from 25 mg and reaching up to 100 mg daily. Other TCAs are imipramine, nortriptyline  and dothiepen.
        Side effects: dry mouth, weight gain, constipation, and urinary retention.
  3. Serotonin norepinephrine reuptake inhibitors (SNRI) – Milnacipran, started off with 15 mg daily and, depending on the resulting pain relief, received up to 100 mg daily for 12 weeks.
  4. Anticonvulsant drugs such as phenytoin, carbamazepine, pregabalin, gabapentin.
    1. Carbamazepine: 100 mg TDS (and 100 mg nocte for elderly patients) and isgradually increased until a therapeutic effect (or side effects) is achieved. The effectivedose may need to be as high as 400 mg TDS, but at this dose various side effects can develop like sedation, ataxiaand gastrointestinal (GIT) upset.
    2. Gabapentin: 300 mg on day 1, 300 mg twice daily on day 2, and300 mg 3 times daily on day 3. May increase dosage up to 1800 mg/d (divided in 3 doses)
    3. Pregabalin: 75 mg/d at bedtime; increase by 75 mg every 5 d to maximum of 300 mg twice daily

Migraine is an extraordinarily common, chronic, intermittently disabling, and usually inherited neurovascular disorder.

  • Caused by vasoconstriction of intracranial vessels (which causes the neurologic symptoms), followed by vasodilation (which results in pounding headache).
  • Series of factors, including the triggeringof neurons in the midbrain that activate the trigeminalnerve system in the medulla, resulting in the release of neuropeptidessuch as substance P.
  • These neurotransmitters activatereceptors on the cerebral vessel walls, causing vasodilationand vasoconstriction. 
  • Fasting.
  • Alcoholic beverages.
  • Hormonal therapy.
  • Caffeine withdrawal.
  • Stress or release from stress.
  • Too much or too little sleep.
  • Menstruation.
  • Fatigue.
  • Exposure to bright lights, loudnoises, smoke, and strong scents.
  • Change in the weather.
  • Acute head injury.
  • Foodstuffs including:
  1. Chocolate.
  2. Aged cheeses.
  3. Processed meats.
  4. Fermented foods.
  5. Aspartame.
  6. Monosodium glutamate.
  7. Citrus fruits.
  8. Nuts.
  • Classic migraine
  • Common migraine
  • Basilar migraine
  • Classic migraine starts with a prodromal aura that is usually visual but that may also be sensoryor motor.
  • The visual aura precedes classic migraine and includes:
  1. Flashing lights or a localized area of depressed vision (scotoma).
  2. Sensitivity to light.
  3. Hemianesthesia.
  4. Aphasia.
  • Aura commonly lasts from 20 to 30 minutes.
  • The aura is followed by an increasingly severe unilateral throbbing headache that is frequently accompanied by nausea and vomiting.
  • The patient characteristically lies down in a dark room and tries to fall asleep.
  • Headaches characteristically last for hours up to 2 or 3 days.
  • Common migraine is not preceded by an aura, but patients may experience irritability or other mood changes.
  • The pain resembles the classic migraine and usually unilateral, pounding, and associated with sensitivityto light and noise.
  • Nausea and vomiting are also common.
  • Most common in young women.
  • Symptoms are primarily neurologic and include aphasia, temporary blindness, vertigo, confusion, and ataxia.
  • These symptoms may be accompanied by an occipital headache.
  1. Acute rescue
  • Analgesics and antiemetics

  Acetylsalicylic acid

1000 mg p.o

  Paracetamol

1000 mg p.o

  Diclofenac

50-75 mg p.o

  Ibuprofen

800-1200 mg p.o

  Ketoprofen

100-200 mg p.o

  Naproxen

500-1000 mg p.o

  Tolfenamic acid

200 mg p.o

Triptans

  • Triptans are usually well-tolerated serotonin receptor agonists.
  • Side effects: dizziness, nausea and vomiting, fatigue, dry mouth and tightness in throat, neck and chest areas, facial flushing and somnolence.

  Almotriptan

12.5 mg, p.o

  Eletriptan

40-80mg,po

  Frovatriptan

2.5mg,po

  Naratriptan

2.5-5mg,po

  Rizatriptan

5-10mg,po

  Sumatriptan

5-100mg,po 6 mg sc

  Zolmitriptan

2.5-5mg, po

  1. Prevention of migraine

Lifestyle management

  • Regularity of biorhythms is the key. The avoidance of relative hypoglycaemia, with a regular, fibre containing diet is probably the most helpful strategy.
  • Change in sleeping times at weekends and irregular shift work may usefully be avoided.

Alice in Wonderland Syndrome, a term coined by Todd in 1955 is a rare migraine aura usually where patientsexperience distortion in body image characterized byenlargement, diminution, or distortion of part of or thewhole body, which they know is not real.

NICO is also known as Alveolar cavitational osteopathosis, Ischemic Osteopathosis, bone marrow oedema. It is a bone disease characterized by degeneration and death of marrow and bone from a slow or abrupt decrease in marrow blood flow.

  1. Commonly associated
    • Coagulation disorder.
    • Alcohol abuse.
    • Trauma.
    • Prednisone.
    • Pregnancy.
    • Sickle cell anaemia.
    • Lupus Erythmatosus.
    • Cancer chemotherapy.
  2. Less commonly associated
    • Tobacco use.
    • Arteriosclerosis.
    • Deep sea diving.
  3. Rarely associated
    • Osteomyelitis.
    •  Starvation.
  • Associated with pain, often with an ill-defined neuralgic or neuropathic character.
  • Ischaemic osteonecrosis most often affects the hips, maxillofacial bones, & knees.
  • NICO prevalence: female > males.
  • Affects women from 35 to 60 years of age.
  • Third molar region mostly affected > any alveolar sites > walls of the sinuses > mandibular condyle.
  • 1/3rd of the patients have more than one site involved & 10% have lesions in all four quadrants.
  • Difficult in describing & localizingpain, which can be intermittent or constant, deep or superficial, aching or sharp, mild or extremely intense.
  • Most often the pain is described as a deep ache or sharp bone pain.
  • It typically begins as quite mild & vague, increasingly slowly in frequency and intensity over months and years, but may also have a sudden onset, especially after a dental procedure using vasoconstrictors in the anesthetic.
  • Pain may roam in the general anatomic area or be referred some distance from the affected bone (neck, shoulder).
  • Osteonecrosis is not visualised in radiographs, but when visible it usually appears as an area of regional osteoporosis or ill- defined radiolucency, often with irregular vertical remnants of lamina dura representing old extraction sites.
  • Occasional lesions show an admixture of irregularly sclerotic & radiolucent areas (ischaemic osteosclerosis), or there may be a faint central sclerotic oval area surrounded by a thick radiolucent circle, which is in turn surrounded by a thick but faint sclerotic ring. (Bull’s Eye Lesion)
  • Antibiotics may temporarily diminish the associated pain of NICO.
  • The diseased marrow must be removed surgically by decortication & curettage.
  • Strong tendency to recur.
  • It is also known as OrolingualParesthesia or Glossodynia or painful tongue, glossopyrosis or ‘burning’ tongue.
  • Painful, burning sensation localized in the tongue.
  • Glossodynia may occur as an isolated symptom or one of a group of oral symptoms, such as taste abnormality, various oral dysthesias including dull, deep, continuous pain of atypical facial pain variety.

It may be of two types-

  • Clinically observable changes in tongue
  • Without observable clinical change
  • Deficiency states such as pernicious anaemia & pellagra.
  •  Diabetes.
  • Gastric disturbances such as hyperacidity or hypoacidity.
  • Psychogenic factors.
  • Trigeminal neuralgia.
  • Periodontal disease.
  • Xerostomia.
  • Hypothyroidism.
  • Referred pain from abscessed teeth or tonsils.
  • Angioneurotic edema.
  • Mercurialism.
  • Moeller’s glossitis.
  • Tongue is the site of paresthetic sensation
  1. Glossodynia- painful tongue
  2. Glossopyrosis-burning tongue
  • Sensation includes most commonly pain, burning, itching &stinging of mucous membrane.
  • Appearance of tissue is usually normal.
  • Common in women past menopause.
  • Rare in children.

Clinical evaluation can be done by:

  • Examination for and elimination of any obvious local irritant (rough teeth, restoration, calculus, irritating food, oral muscular habit and heavy smoking).
  • Role of muscle tension.
  • Allergic to denture base material, metallic restorations and particular foods, medication, mouthwashes & dentifrices.
  • Oral candidiasis.
  • Systemic diseases & deficiency states – untreated Pernicious anaemia& Plummer –Vinson syndrome.
  • In cancer patient, normal volunteers, prisoners of war leads to protein & vitamin deficit – lingual filliform papillary atrophy.
  • Glossodynia may be associated with diabetes mellitus, amyloidosis, multiple myeloma & malignant lesions metastatic to tongue.
  • Neuropathy of lingual nerve due to trauma.
  • Glossopharyngeal neuralgia- episodic pain in posterior part of tongue.
  • Acoustic neuroma – burning sensation in mouth.
  • Lesions of CNS – burning type of intraoral or orofacial pain.
  • Gastric reflux- burning sensation in back of throat.
  • Secondary to coronary insufficiency & cardiac angina.
  • Blood tests – Complete blood count, glucose level, thyroid function, nutritional factors and immune functioning, all of which may provide clues about the source of your mouth discomfort.
  • Oral cultures or biopsies:Taking samples from mouth can tell whether individual have a fungal, bacterial or viral infection.
  • Allergy tests: Allergy test for allergy to certain foods, additives or even substances in dentures.
  • Salivary measurements:Salivary tests too can confirm reduced salivary flow.
  • Gastric reflux tests:These can determine gastroesophageal reflux disease(GERD).
  • Imaging: MRI, CT scan or other imaging tests to check for other health problems.
  • Temporarily stopping medication:If medications that may contribute to mouth discomfort, temporarily stopping those medications, if possible, to see if discomfort goes away. Don’t try this on your own, since it can be dangerous to stop some medications.
  • Psychological questionnaires: Fill out questionnaires that can help determine if patient have symptoms of depression, anxiety or other mental health conditions.
  1. Topical therapy
  • Clonazepam – 1mg Tab to be dissolved & hold in mouth.
  • Lidocaine -2% gel.
  • Capsaicin -0.025% cream.
  • Benzydaminehydrochlorate – 0.15%.
  1. Systemic medications
  • Tricyclic antidepressants: Amitriptyline in doses of 10-150 mg/day, to start with 10 mg at bedtime and increase the dose by 10 mg until oral burning is relieved or side effects occur.
  • Benzodiazepines: Clonazepam exert its effect by acting as a sedative hypnotic 0.25-2 mg dosage/day, 0.25 mg at bedtime, increase dosage by 0.25mg every 4-7 days.
  • Chlordiazepoxide is advised 10-30 mg/day, to start with 5 mg at bedtime and increase the dose to 5 mg every 4-7 days.
  1. Anticonvulsant drug Gabapentin, an anticonvulsant drug, is advised 300-1,600 mg/day; 100 mg at bedtime. The dosage is increased by 100 mg every 4-7 days.
  2. Alpha lipoic acid
  • Administered in doses of 400 mg twice-daily for a month.
  • Alpha-lipoic acid restores glutathione levels, prevents lipid peroxidation, increases the activity of antioxidant enzymes, increases blood flow, glucose uptake, and metabolism in peripheral nerves, along with nerve conduction velocity (NCV)
  • According to the International Headache Society, BMS is an intraoral burning sensation for which no dental or medical cause has been found.
  • International Association for the Study of Pain defined burning mouth syndrome (BMS) “as a burning pain in the tongue and/or other oral mucous membrane in an absence of clinical signs or laboratory findings”.

Based on symptoms burning mouth syndrome can be classified as:

Type 1 BMS: Patients have no symptoms upon waking but symptoms progress throughout the day reaching its peak intensity by evening. Night-timesymptoms are variable. It is linked to systemic disorders like nutritional deficiency and diabetes.

Type 2 BMS: Patients have continuous symptoms throughout the day and are symptomatic at night resulting in sleepless nights. This type is associated with chronic anxiety due to altered sleep pattern and is related to use of antidepressant drugs, which cause xerostomia.

Type 3 BMS: Patients have intermittent symptoms throughout the day with symptom free periods. Usually seen due to anxiety or allergic reactions especially to food allergens.

Based on etiology as:

  • Primary, where etiology is unknown
  • Secondary, where the etiology is known.

Etiology for BMS can be grouped into:

  1. Oral disorders/local factors.
  2. Systemic condition.
  3. Miscellaneous
  1. Oral disorders/local factors include:
    • Denture acrylic allergies/poorly fitting dentures.
    • Para functional habits.
    • Salivary gland dysfunction.
    • Taste dysfunction.
    • Infectious agents.
    • Periodontal diseases.
    • Peripheral nerve damage.
  2. Systemic conditions:
    • Nutritional deficiency/ anemia.
    • Central nervous system disorders.
    • Psychiatric and psychological disorder (depressions, anxiety).
    • Diabetes mellitus/ Hormonal imbalance.
    • Xerostomia.
    • Sjogrens syndrome.
  3. Miscellaneous:
    • Menopause .
    • Food /allergy.
    • Drugs.
  • Occurs most commonly, but not exclusively in females though occurs in men as well.
  • The onset of pain can be either gradual and spontaneous or sudden and related to a precipitating event.
  • Patients usually report that the burning sensation presents its lowest intensity upon waking up, but reappears after the first meal of the day. Once begun, it is continuous, reaching the maximum intensity by late evening.
  • Commonly affects the palate, tongue presenting as glossodynia (painful tongue) and glossopyrosis (burning tongue).
  • Altered taste sensation such as bitter or metallic taste.
  • BMS generally presents as a triad: Mouth pain, alteration in taste, and altered salivation, in the absence of visible mucosal lesions in the mouth.
  • Usually bilateral but can be unilateral as well.
  • Multiple mood and emotional disturbances. 
  1. History and Clinical Examination.
  2. Psychological assessment.
  3. Blood tests: Complete blood cell count, glucose level, thyroid function, nutritional factors and immune function. Oral cultures: For bacterial, viral and fungal infections.
  4. Imaging: Magnetic resonance imaging (MRI), computed tomography (CT) scan or other imaging test to check for other health problems.
  5. Patch tests: To check allergy to certain foods, additives or even denture materials.
  6. Sialometric analysis to measure and check salivary flow.
  7. Gastric reflux tests: To determine GERD.
  8. Biopsy of tongue or oral mucosa.

Management strategies include:

  1. Topical medications.
  2. Systemic medications.
  3. Behavioural interventions.

Topical therapy

  • Clonazepam – 1mg Tab to be dissolved & hold in mouth
  • Lidocaine -2% gel
  • Capsaicin -0.025% cream
  • Benzydaminehydrochlorate – 0.15%

Systemic medications

  • Tricyclic antidepressants: Amitriptyline, in doses of 10-150 mg/day, to start with 10 mg at bedtime and increase the dose by 10 mg until oral burning is relieved or side effects occur.
  • Benzodiazepines: Clonazepam exert its effect by acting as a sedative hypnotic 0.25-2 mg dosage/day, 0.25 mg at bedtime, increase dosage by 0.25 every 4-7 days.

Chlordiazepoxide is advised 10-30 mg/day, to start with 5 mg at bedtime and increase the dose to 5 mg every 4-7 days

  • Anticonvulsant drug: Gabapentin, an anticonvulsant drug, is advised 300-1,600 mg/day; 100 mg at bedtime. The dosage is increased by 100 mg every 4-7 days.
  • Alpha lipoic acid – In doses of 400 mg twice-daily for a month.

The terms ‘‘Eagle’s syndrome’’ or ‘‘Stylohyoid syndrome’’describe a series of symptoms caused by anelongated styloid process and/or the mineralization (ossification or calcification) of part or the entire stylohyoid ligament.

The normal length of the styloid process ranges from 2 to 3 cm.

  1. Theory of Reactive Hyperplasia suggests that if thestyloid process is appropriately stimulated by pharyngealtrauma, ossification may continue from itstip against the stylohyoid ligament.
  2. Theory of Reactive Metaplasia (Eteromorphosis)also includes a traumatic stimulus causingmultiple metaplastic changes to the stylohyoid ligamentand resulting in its partial ossification. Theoccurrence of metaplasia might be attributable tothe presence of osseous centers within these fibrousformations.
  3. Theory of Anatomic Variance – suggests thatstyloid process and the stylohyoid ligament arenormally ossified and that the elongation of the processis simply an anatomical variation. This theoryexplains the early radiological findings of such ossificationin children and young adults who have notundergone any prior cervico-pharyngeal trauma.

Types of Elongation, Patterns of Calcification and Angulation of the Styloid Process

  Type of elongation

  (radiographic appearance)

Pattern of calcification

Angulation of the

styloid process(dgree)

  Type I ¼ elongated (most frequent)

A ¼ calcified outline (most frequent)

Narrow (<65)

  Type II ¼ pseudoarticulated

B ¼ partially calcified

Normal (65–75)

  Type III ¼ segmented

C ¼ nodular

Wide (>75)

 

D ¼ completely calcified

 

According to Eagle, two types of the syndrome:

  • Classic Syndrome-Characterized by pain in  the tonsillar fossa, sometimes  associated with  dysphagia and hypersalivation, and often followed by tonsillectomy.
  • Styloid-Carotid Syndrome: The styloid process compresses the carotid arteries  and exerts particular pressure on its sympathetic fibers. This subtype is not correlated with tonsillectomy
  1. Typically occurs in patients after tonsillectomy, can also occur after any other type of pharyngealsurgery.
  2. A palatable mass may be observed in the tonsillar fossa, its palpation sometimes exacerbatingthe patient’s symptoms.
  3. Symptoms include:
  • Ear pain.
  • Neck pain extending to the oral cavity and the maxilla.
  • Dysphonia.
  • Dysphagia.
  • Odynophagia.
  • Persistent sore throat.
  • Sensation of a foreign body in the pharynx.
  • Painful trismus<25 mm.
  • Vertigo and tinnitus.
  • Pain observed when turning the head or extending thetongue, yawning.

Other symptoms:

  • Tongue pain in general.
  • Sensation of increased salivation.
  • Alterations in taste.
  • Vocal changes.
  • Pain in the upper limbs, chest and temporomandibular joint.
  • Facial paresthesia.
  • Pharyngeal spasm.
  • Pain triggered bythe movement of the mandible.

In the stylo-carotid artery syndrome, an elongated styloid process deviating slightly from its normaldirection can impinge the internal or external carotid artery, stimulating the sympathetic nerveplexus accompanying the artery and causing pain during artery’s palpation.

  • Pain along the artery.
  • Pain in the eye and parietal cephalalgia.
  • Aphasia.
  • Sight disturbances.
  • Syncope episodes.
  • Stimulation of the external carotid artery causes facial pain, mainly in the area underthe eyes.

The diagnosis based on four different parameters:

  1. Clinical manifestations.
  2. Digital palpation of the process in the tonsillar fossa,
  3. Radiological findings
  4. Lidocaineinfiltration test.

Migraine, cluster, chronic tension andcervicogenic headaches, caroticodynia, atypical facialpain,

  1. Conservative treatment:
  • Injection of steroids or long-lasting anesthetics into the lesser cornu ofthe hyoid or the inferior aspect of the tonsillar fossa.
  • Treatment with nonsteroidal anti-inflammatory drugs is considered adjunctivetherapy after surgical treatment for Eagle’ssyndrome.
  • Transpharyngeal manipulation, which involves fracturing the elongated process manually underlocal anaesthesia.
  1. Surgical excision of the elongated styloid process by two different approaches:
  • Extraoral or transcervical
  • Intraoral or transpharyngeal approach.
  • Cardiac distress may sometimes manifest solely as jaw pain or tooth pain.
  • Jaw pain or tooth pain is cyclic.
  • The toothache is increased with physical exertion.
  • Failure of analgesic block to arrest the pain completely is confirming evidence that pain is not from dental origin.
  • Sometimes toothache or jaw pain is associated with chest pain and decreased with nitroglycerine tablet.
  1. Intracranial pain disorders : Neoplasm, aneurysm, abscess, hemorrhage, hematoma, edema
  1. Primary headache disorders (neurovascular disorders) : Migraine, migraine variants, cluster headache, paroxysmal hemicrania,cranial arteritis, carotidynia, tension‑type headache
  1. Neurogenic pain disorders
  • Paroxysmal neuralgias (trigeminal, glossopharyngeal, nervus intermedius, superior laryngeal)
  • Continuous pain disorders (deafferentation, neuritis, postherpetic neuralgia, post‑traumatic, and postsurgical neuralgia)
  • Sympathetically maintained pain
  1. Intraoral pain disorders : Dental pulp, periodontium, mucogingival tissues, tongue.
  1. Temporomandibular disorders : Masticatory muscle, temporomandibular joint, associated structures.
  1. Associated structures : Ears, eyes, nose, paranasal sinuses, throat, lymph nodes, salivary glands,neck.
  1. Gupta R, Mohan V, Mahay P, Yadav PK Orofacial Pain:- A review Dentistry 2016;6:1-6.
  2. Greenberg MS, Glick M Orofacial pain. Oral Medicine Diagnosis & Treatment Burket’s 10th edition Hamilton, Ontario, BC Decker Inc 2003;307-40.
  3. Lund JP, GJ Lavigne GJ, Dubner R, Sessle BJ Orofacial Pain: From Basic Science to Clinical Management, Second Edition.
  4. Jeffrey P. Okeson Bell’s Orofacial Pain 5th edition Quintessence Publishing Company, 1995.
  5. Cummings M, Baldry P. Regional myofascial pain: Diagnosis and management. Best Practice and Research Clinical Rheumatology 2007;21:367-387.
  6. Mehičić GP, Galić N: Odontogenic pain Medical Sciences 2010;34:43-54
  7. Sembulingam k Essentials of medical physiology Nervous system 6th edition jaypee brothers medical publisher 2012;759-901.
  8. Hegarty Anne M, Zakrzewska JM differential diagnosis for orofacial pain, including sinusitis, TMD, trigeminal neuralgia. Dent update 2011;38:396-408.
  9. Migraine and the trigeminal nerve. Migraine Action,Leicester [Internet].2010 [cited on 2015 Feb 19].Available from: http: // www .nhs.uk/ipgmedia/ national /migraine % 20 action /assets / migraineandthetrigeminalnerve.pdf
  10. Jannetta PJ. Arterial compression of the trigeminalnerve at the pons in patients with trigeminal neuralgia.J Neurosurg.1967;26:159-62.
  11. George M, Selvarajan S, Indumathi C. Drug therapyfor trigeminal neuralgia. e-Journal of Dentistry. 2011;1:28-31.
  12. Rhoton AL .The cerebellopontine angle andposterior fossa cranial nerves by retrosigmoidapproach. Neurosurgery. 2000;47:S93-129
  13. Singh P.M., Kaur M., Trikha A An uncommonly common: Glossopharyngeal neuralgia Ann Indian AcadNeurol 2013;16:1-8
  14. Aydin O, Ozturk M, Anik Y,Superior Laryngeal NeuralgiaAfter Acute Laryngitis and TreatmentWith a Single Injection of a Local Anesthetic. Arch Otolaryngol Head Neck Surg 2007;133:934-35
  15. Choi, Jeon RS Neuralgias of the Head: Occipital Neuralgia. Korean Med Sci 2016;31:479-488.
  16. Srivastava R et al. unilateral dermatomal neuralgia after acute herpes zosta infection International Journal of Research in Health and Allied Sciences. 2017;3:70-74.
  17. Sampathkumar P, Drage LA, Martin DP Herpes zoster (shingles) and post hepetic neuralgia. Mayo cllin pro.2009;84:274-280.
  18. Pynn BR, Nish IA Oral surgery: Maxillary Sinusitis: A Review for the Dental Practitioner. Available from: https://www.oralhealthgroup.com/features/oral-surgery-maxillary-sinusitis-a-review-for-the-dental-practitioner/
  19. Mathur M, Goadsby P Cluster headache:-cause and current approaches to treatment. Prescribing in practice. Preecriber 2005;33-39
  20. Comacchio F, Bottin R, Brescia G, Tsilikas K,Volo T, Trgnaghi A Carotidynia:new aspects of a controversial entity. Acta otorhinolayngological italic 2012:32:266-269.
  21. Aydil et al. Carotidynia: Similar Clinical Picture, Different Radiological Findings Turk Arch Otolaryngol 2013; 51: 34-6.
  22. Bell JD, Frank GaillardF et al. Avaible from: Carotidyniahttps:// radiopaeorg/ articles/ carotidynia.
  23. Relatively generalized syndromes. Availablefrom:https:// s3.amazonaws. com/rdcms-iasp/files/production/public/Content/ ContentFolders/ Publications2/ ClassificationofChronicPain/Part_II-A.pdf
  24. Rees RT, Harris M. Atypical odontalgia. Br J Oral Surg. 1979;16:212–218.
  25. Bates RE, Stewart CM. Atypical odontalgia: phantom tooth pain. Oral Surg Oral Med OralPathol 1991;72:479-83.
  26. Marbach JJ. Is phantom tooth pain a deafferentation (neuropathic) syndrome? (part 1):evidence derived from pathophysiology and treatment. Oral Surg Oral Med Oral Pathol.1993;75:95–105.
  27. Melis M, Lobo S.L, Ceneviz C, Zawawi K, Al-Badwi E, Manlony G, Mehta N. A Typical Odotalgia:-A review of literature. Headache 2003;43;1060-1074.
  28. Evans R.W The Clinical features of migrain with and without aura. Practical neurology 2014;26-32.
  29. Kodzhoshalieva B, Vrucak E, Kulovac Causes of treatment of migrain headaches – a literature review. Available from: https://www.theseus.fi/bitstream/handle/10024/130575/Kodzhoshalieva_%20Kulovac_Vrucak.pdf?sequence=1.
  30. Lipton RB et al Cephalgia. International journal of headache2004;24:24-37
  31. Glossodynia (Burning mouth syndrome) Available from: https://pharmacypedia .org/diseases-and-conditions/glossodynia-burning-mouth-syndrome/
  32. Merskey H, Bogduk N. Classification of chronic pain. Seattle (WA): IASP Press; 1994. p. 59-71.
  33. ADA Division of Communications; Journal of the American Dental Association. Burning mouth syndrome. J Am Dent Assoc 2005;136:1191.
  34. Basker RM, Styrdee DW, Davenport JC. Patients with burning mouth: A clinical investigation ofcausative factors including the climacteric and diabetes. Br Dent J 1978;145:9-6.
  35. Scala A, Checchi L, Montevecchi M, Marini I, Giamberardino MA. Update on burning mouth syndrome: overview and patient management. Crit Rev Oral Biol Med 2003;14:275-91.
  36. Soldati A.B., Miguelote. C, Quero C, Pereira R, Santos R, Soares CEagle’s SyndromeArqNeuropsiquiatr 2013;71:264-268.
  37. Piagkou M, Kouladouros K, PiagkosG. Eagle’s Syndrome: A Review of the literatue.Clinical anatomy2009;22:545-58.
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