a. Migraine: See chapter Central Vestibular Disorders. b. Raised intracranial pressure: Headache is generalized
and aggravated by bending and coughing. Headache is worse in morning on awakening. It may awaken patient from sleep. The severity gradually progresses. In later stages it is associated with vomiting and transient loss of vision with sudden change in posture.
tension-type headache
This is the most common type of primary headache. Exploration of the underlying cause of chronic anxiety is important.
Clinical features: Headache is nonpulsatile, diffuse, dull,
aching and band-like. Headache is usually more in occipital and cervical region. Patients often complain of poor concen- tration and other vague nonspecific symptoms.
Aggravating factors: Headache is constant daily and may be
exacerbated by emotional stress, fatigue, noise or glare. It gets worse on touching scalp (pericranial tenderness).
Treatment: Antimigrainous agents are prescribed when
simple analgesics are not effective.
Relaxation techniques: The massage, hot baths and
biofeedback are helpful.
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depression headache
Clinical features: Headache is usually worse on arising in the
morning. Patients may have other symptoms of depression and somatic delusions.
Treatment: It consists of psychiatric consultation and anti-
depressant drugs.
cluster headache
It is mainly the disorder of middle-aged men.
Clinical features: Episodes of severe unilateral pain around
one eye occur daily (more in night) for 4–8 weeks. Episodes awaken the sleeping patient and last for 15 minutes to 3 hours. It is associated with ipsilateral conjunctival conges- tion (red eye), lacrimation, nasal congestion and rhinorrhea. Occasionally, patient may develop Horner’s syndrome, which may be transient or longstanding. Spontaneous remission may last for weeks or months. In cases of chronic cluster headache there is no period of remission.
Triggers: They include alcohol, stress, glare, or specific foods.
Treatment of acute episode: Oral drugs are usually not effec-
tive. Following measures are often effective.
Sumatriptan: Subcutaneous (6 mg) or intranasal (20
mg/spray).
Oxygen: Inhalation of 100% oxygen (12–15 L/min for 15
minutes) via a non-rebreather mask.
Zolmitriptan: 5–10 mg nasal spray. Dihydroergotamine: 0.5–1 mg IM or IV.
Cause Acute (A), subacute (s), Chronic (C), Recurrent (R)
Accompanying diagnostic features Investigations
Tension type headache C and R Anxiety, depression
Migraine A and R Visual/neurological aura, nausea, vomiting
Ocular eye strain C and R Impaired visual acuity Refractive error Glaucoma A and R Misting of vision, haloes around
objects
Intraocular tension
Retrobulbar neuritis A Unilateral blindness Visual evoke response Sinusitis A, R Cold and purulent nasal discharge CT scan PNS
Post-traumatic A Head injury CT scan head Drugs A and C Vasodilator drugs
Benign intracranial hypertension
S and R Vomiting, papilloedema CSF pressure monitoring
Intracranial hemorrhage A (Instant onset) Vomiting, neck rigidity, impaired consciousness
CT scan brain
Meningitis and encephalitis
A and S (gradual onset) Vomiting, neck rigidity, impaired consciousness, fever
Intracranial tumor and chronic subdural hematoma
S and R Vomiting, papilloedema, impaired consciousness, focal features
MRI/CT Brain
Cluster headache A and R Lacrimation, rhinorrhea
Temporal arteritis S Thickened, tender scalp arteries, jaw claudication
ESR, temporal artery biopsy
Cervical spondylosis C and R Pain in neck, shoulder and arm X-ray cervical spine
tablE 7 Common causes of headache and their features
Xylocaine viscous: 1 mg of 4–6% solution intranasally.
Prophylactic agents: They include cyproheptadine, lithium
carbonate, verapamil (240–960 mg daily), topiramate (100–400 mg daily) and methysergide (2–12 mg daily).
Transitional therapy: Prophylactic agents are not imme-
diately effective therefore following drugs are used in transitional therapy.
Ergotamine tartarate: Rectal suppository (0.5–1 mg) at
night or twice daily, 2 mg daily orally, or 0.25 mg subcu- taneously 3 times daily for 5 days per week.
Prednisone: 60 mg daily for 5 days followed by gradual
withdrawal.
Dihydroergotamine: 9.25 mg IV over several days or 0.5
mg IM twice daily.
Xylocaine and corticosteroid: Greater occipital nerve
block with local injection of xylocaine and corticoste- roid.
Post-traumatic headache
Clinical features: This constant dull headache develops
within a day or so following closed head injury, may worsen over weeks and then gradually subsides. Throbbing sensa- tion may be localized, lateralized, or generalized. Headache developing after 2 weeks of injury is usually not related to head injury.
Associated features: Patients may have associated
nausea, vomiting, or scintillating scotomas. The head- ache is associated with lightheadedness, irritability,
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important. If simple analgesics fail then amitriptyline, anti- seizure drugs, propranolol, or ergot derivatives are used.
cough headache
This is usually a self-limiting disease. In some patients it may persist for several years.
Clinical features: This transient (few minutes or less) but
severe headache is produced by coughing, straining, sneezing and laughing.
CT/MRI scans: They should be done in all patients to rule
out space occupying intracranial lesions and Arnold-Chiari malformation. CT/MRI may be repeated annually as a small lesion may not show initially.
Treatment: Lumbar puncture may alleviate the symptoms
completely. Indomethacin (75–150 mg daily) is effective in some patients.
giant cell (temporal or cranial) arteritis
In addition to the superficial temporal, other arteries which are often affected are vertebral, ophthalmic and posterior ciliary arteries. Early diagnosis and treatment can prevent blindness which is usually permanent.
Clinical features: This unilateral severe throbbing headache
occurs in elderly people. The headache is often associated or preceded by myalgia, malaise, anorexia and weight loss. The superficial temporal artery becomes thickened, tender and nonpulsatile. Jaw claudication (pain during chewing and talking) is pathognomonic. Many patients present with blindness (transient or permanent) and diplopia. Some patients may develop stroke, hearing loss, myelopathy and neuropathy.
Biopsy: Prompt temporal artery biopsy (at least 2 cm in length)
is important. Biopsy shows lymphocytes, histiocytes, plasma cells and giant cells in media and adventitia.
Treatment: On clinical suspicion immediately initiate pred-
nisone (60 mg/day for 1 month before tapering). In cases of blindness intravenous pulse Methylprednisolone (1 gm daily for 3 days) is given. When tapering prednisone, erythrocyte sedimentation rate (ESR) or C-reactive protein is a useful but not absolute guide.
Aspirin: Low dose aspirin (up to 81 mg/day orally) may
prevent blindness and stroke.
Methotrexate: It is modestly effective.
Anti-tumor necrosis factor (TNF) therapies: They are
not effective.
Complications: Thoracic aortic aneurysm can result in aortic
regurgitation, dissection and rupture.
stabbing and shooting facial pain occur in the region of one or more divisions (ophthalmic, maxillary and mandibular) of the trigeminal nerve. Pain may radiate towards ear, eye, mouth or nostril. Precipitating factors include chewing, speaking, face washing, tooth-brushing, cold winds, or touching of trigger spots such as upper lip or gum. Spontaneous remissions for several months or longer are not uncommon. Neurological examination is normal.
Differential diagnosis: In a young patient multiple sclerosis
must be suspected. Evoked potential testing and CSF examination may be corroborative. CT/MRI scan is done to rule out posterior cranial fossa tumor.
Treatment
Carbamazepine (600–1200 mg/day in 3–4 divided
doses): It is usually very effective. They need monitoring of CBC and liver function tests. Oxcarbazepine also offers good results.
Phenytoin (200–400 mg/day): It is used when
Carbamazepine or oxcarbazepine are not effective or not tolerated.
Baclofen (10–20 mg 3 or 4 times a day): It may be used
either alone in combination with above molecules.
Gabapentine (900–2400 mg/day in 3 divided doses) or
pregabalin (up to 300 mg/day): It is used when above medicines do not work or patient is suffering from multiple sclerosis.
Noninvasive procedures:
– Radiofrequency rhizotomy: This simple procedure
is preferred in elderly patients with a limited life expectancy.
– Trigeminal root gamma radiosurgery: This nonin-
vasive procedure is successful in 80% of patients.
Exploration of posterior cranial fossa: Simple decom-
pression and separation of anomalous vessel from the nerve root usually produce lasting relief. The anomalous artery or vein impinging on trigeminal nerve root is usually not seen on CT, MRI or arteriograms. It is not indicted in patients with multiple sclerosis.
atypical facial Pain
Clinical features: Diffuse, dull, persisting pain occurs in depres-
sive young or middle aged woman. It may be unilateral or bilateral. Initially the burning pain has restricted distribution but soon spreads to rest of the face. In some patients pain may involve other side, neck or occipital region.
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Treatment: Patients may be given analgesics, tricyclic anti-
depressants, carbamazepine, oxcarbazepine or phenytoin but the response is often not satisfactory.
glossopharyngeal neuralgia
This disorder is uncommon.
Etiology: Usually no structural abnormality is found. Multiple
sclerosis may be the cause in some patients.
Clinical features: This neuralgic pain (similar in quality to
trigeminal neuralgia) occurs usually in tonsillar fossa. It may occur deep in the ear or at base of the tongue. The precipitating factors may be swallowing, chewing, talking, or yawning. It may be accompanied by syncope.
Treatment: Pharmacological treatment is similar to
trigeminal neuralgia and should be given a trial. Microvascular decompression is indicated when medical treatment fails.
Post-herpetic neuralgia
About 15% patients of shingles (Herpes zoster) develop postherpetic neuralgia.
Risk factors: They include old age, severe rash (long duration,
painful and scarring), involvement of ophthalmic division of trigeminal nerve and delayed acyclovir therapy.
Clinical features: Dull, burning, persisting (occasionally
paroxysm) pain occurs after herpetic lesions. It affects the trigeminal area especially ophthalmic division. Healed lesion with scars is associated with sensory loss.
Treatment: It is essentially medical. In addition to the
medical treatment (carbamazepine, phenytoin, gabapen- tine and pregabalin) mentioned in the trigeminal neuralgia it includes the following:
Amitriptyline and perphenazine: If simple analgesics are
not effective tricyclic antidepressant (amitriptyline up to 100–150 mg/day) in conjunction with phenothiazine (perphenazine 2–8 mg/day) is usually effective.
Gabapentin and morphine: The combination of gaba-
pentin and morphine taken orally is more effective than taken individually.
Topical applications: Capsaicin cream (0.025%) and
lidocaine (5%) are worthy of trial.
Prevention: Live-attenuated zoster vaccine to elderly
patients (> 60 years) prevents occurrence of herpes zoster and markedly reduces morbidity.
tEmPOrOmandibular (craniOmandibu- lar) diSOrdErS
TMD consists of not only the internal derangement of temporomandibular joint (TMJ) but also areas extrinsic to TMJ. Temporomandibular (craniomandibular) disorders (TMD) patients present with musculoskeletal symptoms such as diffuse facial pain with jaw movements, limitation of mandib- ular movement and masticatory muscle and TMJ tenderness. Patients with internal derangement of TMJ (disc displacement, osteoarthrosis, inflammation and congenital, developmental, traumatic and neoplastic disorders) present with well localized pain.
Etiology
The causes of TMD and TMJ disorders are shown in Table 8. They occur due to the misalignment of one TMJ. TMD may be caused by malocclusion, abnormal bite, or faulty dentures.
clinical features
Patients usually have dental loss with altered bite. Other features are following:
Aching pain occurs around the ear that is aggravated by
chewing.
Limitation in jaw movements. Deviation in mandibular motion.
Locking of jaw in open or closed position. Clicking sound/crepitus within TMJ. Masticatory muscles pain and tenderness.
myogenic (masticatory muscles) disorders
Temporomandibular disorder patients with myogenic pain usually have normal TMJ. The limitation of jaw movement is due to muscle pain and stiffness. The pain is usually due to hyperfunction. Myogenic disorders include myofascial pain, fibrositis, muscle splinting (trismus), spasm and swelling (myositis), contracture, bruxism, hypertrophy and dyskinesia. There is usually no evidence (clinical and radiographic) of internal derangement of TMJ.
Predisposing factors: Nocturnal or diurnal bruxism (grinding
or clenching) is very common. It is more during physical or emotional stress. This hyperactivity results in muscle fatigue and spasm. This strain which is due to overuse or improper use must be treated as such.
Clinical features: The most common complaint of the
patients is diffuse facial pain. According to the involvement of muscles, patients with myogenic disorders may have following symptoms.
TMJ disorders (internal derangement) Displacement, dysfunction and perforation of disc, adhesions and degenerative joint disease
Myogenic (masticatory muscles) disorders Muscle trismus or splinting
Chronic mandibular hypomobility Muscular and capsular fibrosis, bony ankylosis and fusion, adhesions and elongation of coronoid process
Chronic mandibular hypermobility Subluxation and dislocation
Inflammatory disorders Synovitis, capsulitis, hyperuricemia and degenerative, infectious, traumatic and rheumatoid arthritis
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giant cell arteritis.
meniscal displacement
Disk displacement can be a cause or result of osteoarthritis. Both the disorders can be present independently. About 20% of the population may have some form of disk displacement without pain or dysfunction.
imaging Studies
1. OPG: Panoramic view shows only gross disease (degenera- tive and ankylosis) and general joint configuration. 2. CT scan: It is ideal for fine osseous and fibrous evaluation.
3. MRI: It is ideal for evaluating disk morphology and position
and early degenerative bone changes.
treatment
It consists of the treatment of the underlying TMJ disorder. Most TMD patients respond to nonsurgical therapy that includes rest, and medical, physical and splint therapies. Surgical treatment is indicated only for internal derangement of the TMJ.
Restricted mouth opening and soft diet: Limitation of function
reduces painful loads on the inflammatory tissues.
Analgesics: Non-narcotic analgesics (acetaminophen) and
nonsteroidal anti-inflammatory drugs (NSAIDs) constitute the initial therapy. When a particular NSAID is not effective then a different one should be used. Long-term or high doses of NSAIDs may cause gastrointestinal bleeding, ulcers,
metaxalone (800 mg tds).
Anxiolytics: Benzodiazepines are sedatives and reduce
anxiety and muscle hyperactivity. The commonly used agents include clonazepam (0.5–1 mg 1–4 times/day), diazepam (2–10 mg 1–4 times/day) and alprazolam (0.5 mg 1–3 times/day).
Antidepressants: Tricyclic and serotonin-reuptake inhibi-
tors are useful in the management of chronic pain. The commonly used agents include amitriptyline (10–25 mg/ day), imipramine (10–25 mg/day), fluoxetine (5 mg/day), sertraline (50 mg/day), citalopram (20 mg/day), venlafaxine (75 mg/day), nortriptyline (10–25 mg/day), bupropion (100 mg bd) and paroxetine (20 mg/day).
Narcotics: They are used in chronic pain patients. The
caution is required as they are habit forming agents.
Bite-appliance (splint) therapy: The splint is worn on the teeth
and stabilizes the occlusion (in bruxism) and reduces the load. It relieves acute myogenic and TMJ pain.
Other therapies: Physical therapy, behavioral training and
stress management are effective in many patients.
Surgery: Surgical correction is indicated only when internal
derangement symptomatic TMJ patients do not respond to above mentioned modalities of treatment. The details of surgical options, which include arthrocentesis, arthroscopy, arthrotomy (arthroplasty) and meniscal repair (plication), are beyond the scope of this chapter.
1. Ent examination: Keep a specific order with clinical examination and within each area such as ear, nose, mouth, pharynx
and larynx, face and scalp, neck and neurologic exam. It ensures complete examination and avoids missing anything.
2. inadvertent injury: When examining ear, nose and throat, your hand that is holding the instrument should be stabilized
against the patient. This practice prevents inadvertent injury upon sudden patient movement.
3. assurance: Before examination always describe to the patient what you intend to do. Assure the patient that the procedure
will not hurt him/her. Again assure the patient that if anything bothers then s/he should tell you.
4. height: Adjust the patient’s chair height. Patient’s head should be little higher than the examiner.
5. Oral and pharyngeal examination: It also includes transoral palpation. It is important because certain lesions such as
submucosal mass/nodule of carcinoma tongue can be felt and not seen.
6. headache: The common causes in women are migraine, tension and trigeminal. 7. diurnal headache: It is a feature of acute frontal sinusitis.
8. Vacuum headache: It is associated with frontal sinus.
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furthEr rEading
1. Alper CM, Myeres Eugene N, Eabling DE. Decision Making in Ear, Nose and Throat Disorders. Philadelphia: WB Saunders; 2002. 2. American Academy of Otolaryngology-Head and Neck Surgery, Inc.(online). Available from www.entnet.org.
3. American Board of otolaryngology (online). Available from www.aboto.org.
4. Bickley LS, Szilagyi PG. Bates’ Guide to Physical Examination and History taking, 8th edition. Philadelphia: Lippincott; 2003. pp. 144-208. 5. Bluestone CD, Klein JO. Methods of examination: clinical examination. In: Bluestone CD (Ed). Pediatric Otolaryngology, 4th edition.
Philadelphia: WB. Saunders; 2002. pp. 172-86.
6. Gaur K, Kasliwal N, Bhandari A, et al. Changing trends in otorhinolaryngological diseases at a non-government clinic in Jaipur. Indian J Otolaryngol Head Neck Surg. 2009;61:173-8.
7. Goldstein JC. Rise of medical specialization and organizations affecting otolaryngology. Laryngoscope. 2001;111:1119-27.
8. Haddad J. Methods of examination. In: Bluestone CD (Ed). Pediatric otolaryngology, 4th edition. Philadelphia: WB Saunders; 2002. pp. 1621-8.
9. Kaluskar SK. Evolution of rhinology. Indian J Otolaryngol Head Neck Surg. 2008;60:101-5.
10. Lawrence TWC, Postic WP, Handler SD. Methods of examination. In: Bluestone CD (Ed). Pediatric Otolaryngology, 4th edition. Philadelphia: WB. Saunders; 2002. pp. 1109-19.
11. Lee KJ. Essential Otolaryngology: Head and Neck Surgery, 8th edition. New York: McGraw Hill; 2002.
12. Rahber R, Healy GB. Methods of examination. In: Bluestone CD (Ed). Pediatric Otolaryngology, 4th edition. Philadelphia: WB. Saunders; 2002. pp. 887-96.
13. Saha N, Chandra S, Mondal PK, et al. Emergency otorhinolaryngological cases in medical college, Kolkata-A Statistical analysis. Indian J Otolaryngol Head Neck Surg. 2005;57:219-25.
14. Sarkar S, Roychoudhury A, Roychaudhri B.K. Foreign bodies in ENT in a teaching hospital in Eastern India. Indian J Otolaryngol Head Neck Surg. 2010;62:118-20.
15. Seidel HM, Ball JW, Danis JE, et al. Mosby’s Guide to Physical Examination, 5th edition. St. Louis: Mosby; 2003. pp. 313-55.
16. Sharma K, Sharma S, Chander D. Evaluation of audio-rhinological changes during pregnancy. India J Otolaryngol Head and Neck Surg. 2011;63:74-8.
17. Sinha V, Johri S, George A. Congenital anomalies in ENT. Indian J Otolaryngol Head Neck Surg. 2001;53:326-7. 18. Sinha V. Practical ENT. Mumbai: National Book Depot; 2009.
Man begins to struggle and fight against nature. He makes many mistakes, he suffers. But eventually, he conquers nature and realizes his freedom. When he is free, nature becomes his slave.
—Swami Vivekananda