SINUSITIS

Sinusitis refers to an inflammatory condition involving the four paired structures surrounding the nasal cavities. Although most cases of sinusitis involve more than one sinus, the maxillary sinus is most commonly involved; Each sinus is lined with a respiratory epithelium that produces mucus, which is transported out by ciliary action through the sinus ostium and into the nasal cavity. Normally, mucus does not accumulate in the sinuses, which remain sterile despite their adjacency to the bacterium-filled nasal passages. When the sinus ostia are obstructed, however, or when ciliary clearance is impaired or absent, the secretions can be retained, producing the typical signs and symptoms of sinusitis.


Acute Sinusitis

Acute sinusitis—defined as sinusitis of <4 weeks' duration—constitutes the vast majority of sinusitis cases. Most cases are diagnosed in the ambulatory care setting and occur primarily as a consequence of a preceding viral URI. Differentiating acute bacterial and viral sinusitis on clinical grounds is difficult. Therefore, it is perhaps unsurprising that antibiotics are prescribed frequently (in 85–98% of all cases) for this condition. Etiology A number of infectious and noninfectious factors can contribute to acute obstruction.non infectious factors include allergic rhinitis,barotrauma or chemical irrtants.Illnesses such as nasal and sinus tumors (e.g., squamous cell carcinoma) or granulomatous diseases (e.g., Wegener's granulomatosis or rhinoscleroma) can also produce obstruction of the sinus ostia, while conditions leading to altered mucus content (e.g., cystic fibrosis) can cause sinusitis through impaired mucus clearance. viral sinusitis is far more common than bacterial.A number of bacteria may also cause sinusitis. the viruses most commonly isolated—both alone and with bacteria—have been rhinovirus, parainfluenza virus, and influenza virus Clinical Manifestations most of the sinusitis patients presents with symptoms of upper respiratory tract infections. Common presenting symptoms of sinusitis include nasal drainage and congestion, facial pain or pressure, and headache. Thick, purulent or discolored nasal discharge is often thought to indicate bacterial sinusitis but also occurs early in viral infections such as the common cold and is not specific to bacterial infection. Other nonspecific manifestations include cough, sneezing, and fever. Tooth pain, most often involving the upper molars, is associated with bacterial sinusitis, as is halitosis. In acute sinusitis, sinus pain or pressure often localizes to the involved sinus (particularly the maxillary sinus) and can be worse when the patient bends over or is supine Table 31-1 Guidelines for the Diagnosis and Treatment of Acute Sinusitis Age Group Diagnostic Criteria Treatment Recommendationsa Adults Moderate symptoms (e.g., nasal purulence/ congestion or cough) for >7 d or Initial therapy
Severe symptoms of any duration, including unilateral/focal facial swelling or tooth pain Amoxicillin, 500 mg PO tid or 875 mg PO bid, or
TMP-SMX, 1 DS tablet PO bid for 10–14 d
Exposure to antibiotics within 30 d or >30% prevalence of penicillin-resistant S. pneumoniae
Amoxicillin, 1000 mg PO tid, or
Amoxicillin/clavulanate (extended release), 2000 mg PO bid, or
Antipneumococcal fluoroquinolone (e.g., levofloxacin, 500 mg PO qd)
Recent treatment failure
Amoxicillin/clavulanate (extended release), 2000 mg PO bid, or
Amoxicillin, 1500 mg bid, plus clindamycin, 300 mg PO qid, or
Antipneumococcal fluoroquinolone (e.g., levofloxacin, 500 mg PO qd)
Children Moderate symptoms (e.g., nasal purulence/congestion or cough) for >10–14 d or Initial therapy
Severe symptoms of any duration, including fever (>102°F), unilateral/focal facial swelling or pain Amoxicillin, 45–90 mg/kg qd (up to 2 g) PO in divided doses (bid or tid), or
Cefuroxime axetil, 30 mg/kg qd PO in divided doses (bid), or
Cefdinir, 14 mg/kg PO qd
Exposure to antibiotics within 30 d, recent treatment failure, or >30% prevalence of penicillin-resistant S. pneumoniae
Amoxicillin, 90 mg/kg qd (up to 2 g) PO in divided doses (bid), plus clavulanate, 6.4 mg/kg qd PO in divided doses (bid) (extra-strength suspension), or
Cefuroxime axetil, 30 mg/kg qd PO in divided doses (bid), or
Cefdinir, 14 mg/kg PO qd


CHRONIC SINUSITIS

Chronic sinusitis is characterized by symptoms of sinus inflammation lasting >12 weeks. This illness is most commonly associated with either bacteria or fungi, and clinical cure in most cases is very difficult. Many patients have undergone treatment with repeated courses of antibacterial agents and multiple sinus surgeries, increasing their risk of colonization with antibiotic-resistant pathogens and of surgical complications. Patients often suffer significant morbidity, sometimes over many years.

in chronoc sinusitis infection is thought to be due to impairment of mucociliary clearence.Chronic fungal sinusitis is a disease of immunocompetent hosts and is usually noninvasive, although slowly progressive invasive disease is sometimes seen. Noninvasive disease, which is typically associated with hyaline molds such as Aspergillus species and dematiaceous molds such as Curvularia or Bipolaris species, can present as a number of different scenarios

Chronic Sinusitis: Treatment

Treatment of chronic bacterial sinusitis can be challenging and consists primarily of repeated culture-guided courses of antibiotics, sometimes for 3–4 weeks at a time; administration of intranasal glucocorticoids; and mechanical irrigation of the sinus with sterile saline solution. When this management approach fails, sinus surgery may be indicated and sometimes provides significant, albeit short-term, alleviation. Treatment of chronic fungal sinusitis consists of surgical removal of impacted mucus. Recurrence, unfortunately, is common.

VERTIGO

vertigo is a feeling of unstability to the patient where the world seems to be rotating.
vertigo is mainly caused by peripheral and central disorders.peripheral disorders means that involves the vestibular component in the ear.central disorders include which involve central nervous system after the entrance of vestibular nerve in the brain stem and othern central nervous systemm pathways.

vestibular disorders

PERIPHERAL (lesions of end organs vestibular nerve)

meniere's disease

benign paroxysmal
positional vertigo


labyrynthitis

vestibulotoxic drugs


head trauma

perilymph fistula

syphilis

acoustic neuroma

vestibular neuronitis


CENTRAL(lesions of brain stem and central connections)

Vertebro basilar insufficiency

posterior inferior cerebellar artery syndrome

basilar migraine

cerebellar disease

multiple sclerosis

tumours of brain stem and fourth ventricle

epilepsy

cervical vertigo

MENIERE'S DISEASE:charecterized by vertigo,fluctuating hearing loss and tinnitus.vertigo is of sudden onset lasts for a few minutes to 24 hrs.
TREATMENT:VESTIBULAR SEDATIVES are very much useful.but general measures like cessation of smoking,low salt diet should be followed.

BENIGN PAROXYSMAL POSITIONAL VERTIGO:it is charecterized by vertigo when the head is kept in a particular position.history of head trauma and ear infection may be present
this conditin can be treated by performing EPLEY'S MANOEUVRE

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Back ache

Back symptoms are the most commom cause of disability in patients above 45 years of age.
Types of back pain
Local pain is caused by stretching of pain-sensitive structures that compress or irritate sensory nerve endings. The site of the pain is near the affected part of the back.

Pain referred to the back may arise from abdominal or pelvic viscera. The pain is usually described as primarily abdominal or pelvic but is accompanied by back pain and usually unaffected by posture. The patient may occasionally complain of back pain only.

Pain of spine origin may be located in the back or referred to the buttocks or legs. Diseases affecting the upper lumbar spine tend to refer pain to the lumbar region, groin, or anterior thighs. Diseases affecting the lower lumbar spine tend to produce pain referred to the buttocks, posterior thighs, or rarely the calves or feet. Provocative injections into pain-sensitive structures of the lumbar spine may produce leg pain that does not follow a dermatomal distribution. This "sclerotomal" pain may explain some cases of back and leg pain without evidence of nerve root compression.

Radicular back pain is typically sharp and radiates from the lumbar spine to the leg within the territory of a nerve root . Coughing, sneezing, or voluntary contraction of abdominal muscles (lifting heavy objects or straining at stool) may elicit the radiating pain. The pain may increase in postures that stretch the nerves and nerve roots. Sitting stretches the sciatic nerve (L5 and S1 roots) because the nerve passes posterior to the hip. The femoral nerve (L2, L3, and L4 roots) passes anterior to the hip and is not stretched by sitting. The description of the pain alone often fails to distinguish between sclerotomal pain and radiculopathy.

Pain associated with muscle spasm, although of obscure origin, is commonly associated with many spine disorders. The spasms are accompanied by abnormal posture, taut paraspinal muscles, and dull pain.



Causes of Back and Neck Pain



Congenital/developmental
Spondylolysis and spondylolisthesisa
Kyphoscoliosisa

Spina bifida occultaa

Tethered spinal corda

Minor trauma
Strain or sprain
Whiplash injuryb

Fractures
Traumatic—falls, motor vehicle accidents
Atraumatic—osteoporosis, neoplastic infiltration, exogenous steroids
Intervertebral disk herniation
Degenerative
Disk-osteophyte complex
Internal disk disruption
Spinal stenosis with neurogenic claudicationa

Uncovertebral joint diseaseb

Atlantoaxial joint disease (e.g., rheumatoid arthritis)a

Arthritis
Spondylosis
Facet or sacroiliac arthropathy
Autoimmune (e.g., anklyosing spondylitis, Reiter's syndrome)
Neoplasms—metastatic, hematologic, primary bone tumors
Infection/inflammation
Vertebral osteomyelitis
Spinal epidural abscess
Septic disk
Meningitis
Lumbar arachnoiditisa

Metabolic
Osteoporosis—hyperparathyroidism, immobility
Osteosclerosis (e.g., Paget's disease)
Vascular
Abdominal aortic aneurysm
Vertebral artery dissectionb

Other
Referred pain from visceral disease
Postural
Psychiatric, malingering, chronic pain syndromes



aLow back pain only.

bNeck pain only.

STRAIN AND SPRAIN

The terms low back sprain, strain, or mechanically induced muscle spasm refer to minor, self-limited injuries associated with lifting a heavy object, a fall, or a sudden deceleration such as in an automobile accident. These terms are used loosely and do not clearly describe a specific anatomic lesion. The pain is usually confined to the lower back, and there is no radiation to the buttocks or legs. Patients with paraspinal muscle spasm often assume unusual postures

Lumbar Disk Disease

This is a common cause of chronic or recurrent low back and leg pain . Disk disease is most likely to occur at the L4-L5 and L5-S1 levels, but upper lumbar levels are involved occasionally. The cause is often unknown; the risk is increased in overweight individuals. Disk herniation is unusual prior to age 20 and is rare in the fibrotic disks of the elderly. Degeneration of the nucleus pulposus and the annulus fibrosus increases with age and may be asymptomatic or painful. Genetic factors may play a role in predisposing some patients to disk degeneration. The pain may be located in the low back only or referred to the leg, buttock, or hip. A sneeze, cough, or trivial movement may cause the nucleus pulposus to prolapse, pushing the frayed and weakened annulus posteriorly. With severe disk disease, the nucleus may protrude through the annulus (herniation) or become extruded to lie as a free fragment in the spinal canal.


TREATMENT


treatment of the back pain depends on the underlying condition.prains and strain may be releived b y simple rest of the involved muscle.disk prolapse in some conditions need surgery.cervical spondylosis is very prevalent now a days and it is charecterized by relapses and emissions even we use the treatment

cases in paediatric surgery,trichobezoar

in my internship..now i'm posted in paediatric surgery.2 days back v admitted a case,12 yrs old female child from emergency for acute intestinal obstruction for surgery.all of us thought that it might be a case of bands or volvulus but surprisingly it was a case of trichobezoar in small bowel.nobody,even her parents knew that she was eating hair.they just thought that she was playing with comb.

Fever - Wikipedia, the free encyclopedia

Fever - Wikipedia, the free encyclopedia

FEVER

BOdy temperature is maintained by hypothalamus.A normal body temperature is ordinarily maintained, despite environmental variations, because the hypothalamic thermoregulatory center balances the excess heat production derived from metabolic activity in muscle and the liver with heat dissipation from the skin and lungs. According to studies of healthy individuals 18–40 years of age, the mean oral temperature is 36.8° ± 0.4°C (98.2° ± 0.7°F), with low levels at 6 A.M. and higher levels at 4–6 P.M. The maximum normal oral temperature is 37.2°C (98.9°F) at 6 A.M. and 37.7°C (99.9°F) at 4 P.M.; these values define the 99th percentile for healthy individuals.
Rectal temperatures are generally 0.4°C (0.7°F) higher than oral readings. The lower oral readings are probably attributable to mouth breathing, which is a factor in patients with respiratory infections and rapid breathing.
What is a fever?

Fever refers to an elevation in body temperature. Technically, any body temperature above the normal oral measurement of 98.6 F (37 C) or the normal rectal temperature of 99 F (37.2 C) is considered to be elevated. However, these are averages, and one's normal body temperature may actually be 1 F (0.6 C) or more above or below the average of 98.6 F. Body temperature can also vary up to 1 F (0.6 C) throughout the day.

Fever is not considered medically significant until body temperature is above 100.4 F (38 C). Anything above normal but below 100.4 F (38 C) is considered a low-grade fever. Fever serves as one of the body's natural defenses against bacteria and viruses which cannot live at a higher temperature. For that reason, low fevers should normally go untreated, unless accompanied by troubling symptoms.

Also, the body's defense mechanisms seem to work more efficiently at a higher temperature. Fever is just one part of an illness, many times no more important than the presence of other symptoms such as cough, sore throat, fatigue, joint pains or aches, chills, nausea, etc.

Fevers of 104 F (40 C) or higher demand immediate home treatment and subsequent medical attention, as they can result in delirium and convulsions, particularly in infants and children.

Fever should not be confused with hyperthermia, which is a defect in your body's response to heat (thermoregulation), which can also raise the body temperature. This is usually caused by external sources such as being in a hot environment.
Types
The pattern of temperature changes may occasionally hint at the diagnosis:
Continuous fever: Temperature remains above normal throughout the day and does not fluctuate more than 1 °C in 24 hours, e.g. lobar pneumonia, typhoid, urinary tract infection, brucellosis, or typhus. Typhoid fever may show a specific fever pattern, with a slow stepwise increase and a high plateau. (Drops due to fever-reducing drugs are excluded.)
Intermittent fever: The temperature elevation is present only for a certain period, later cycling back to normal, e.g. malaria, kala-azar, pyaemia, or septicemia.[citation needed]
Quotidian fever, with a periodicity of 24 hours, typical of Malaria
Tertian fever (48 hour periodicity), typical of Malaria
Quartan fever (72 hour periodicity), typical of Plasmodium malariae).
Remittent fever: Temperature remains above normal throughout the day and fluctuates more than 1 °C in 24 hours, e.g., infective endocarditis.
Pel-Ebstein fever: A specific kind of fever associated with Hodgkin's lymphoma, being high for one week and low for the next week and so on. However, there is some debate as to whether this pattern truly exists.[12]
A neutropenic fever, also called febrile neutropenia, is a fever in the absence of normal immune system function. Because of the lack of infection-fighting neutrophils, a bacterial infection can spread rapidly; this fever is, therefore, usually considered to require urgent medical attention. This kind of fever is more commonly seen in people receiving immune-suppressing chemotherapy than in apparently healthy people.
Febricula is an old term for a low-grade fever, especially if the cause is unknown, no other symptoms are present, and the patient recovers fully in less than a week.[13

Management

Fever should not necessarily be treated.[28] Most people recover without specific medical attention.[29] Although it is unpleasant, fever rarely rises to a dangerous level even if untreated. Damage to the brain generally does not occur until temperatures reach 42 °C (107.6 °F), and it is rare for an untreated fever to exceed 105 °F (41 °C).[28]
In general, people are advised to keep adequately hydrated, as the most significant risk of complications is dehydration. Water is generally used for this purpose. The risk of hyponatremia induced by increased fluid intake can be reduced through the use of appropriately formulated oral rehydration solutions.[citation needed] Other options include ice pops, juice, and other non-alcoholic drinks.
Some limited evidence supports sponging or bathing feverish children with tepid water.[30] The use of a fan or air conditioning may somewhat reduce the temperature and increase comfort. If the temperature reaches the extremely high level of hyperpyrexia, aggressive cooling is required.[15]
[edit]Medications
The antipyretic ibuprofen is effective in reducing fevers in children.[31] It is more effective than acetaminophen (paracetamol) in children. Ibuprofen and acetaminophen may be safely used together in children with fevers.[32][33] The efficacy of acetaminophen by itself in children with fevers has been questioned.[34] Ibuprofen is also superior to aspirin in children with fevers,[35] which is not usually recommended in children due to the risk of Reye's syndrome

Abdominal pain - Wikipedia, the free encyclopedia

Abdominal pain - Wikipedia, the free encyclopedia

abdominal pain

HEADACHE

.

Headache: Introduction Headache is among the most common reasons that patients seek medical attention. Diagnosis and management is based on a careful clinical approach that is augmented by an understanding of the anatomy, physiology, and pharmacology of the nervous system pathways that mediate the various headache syndromes.

General Principles A classification system developed by the International Headache Society characterizes headache as primary or secondary Primary headaches are those in which headache and its associated features are the disorder in itself, whereas secondary headaches are those caused by exogenous disorders. Primary headache often results in considerable disability and a decrease in the patient's quality of life. Mild secondary headache, such as that seen in association with upper respiratory tract infections, is common but rarely worrisome. Life-threatening headache is relatively uncommon, but vigilance is required in order to recognize and appropriately treat patients with this category of head pain. Common Causes of Headache Primary Headache Secondary Headache Type % Type % Migraine 16 Systemic infection 63 Tension-type 69 Head injury 4 Cluster 0.1 Vascular disorders 1 Idiopathic stabbing 2 Subarachnoid hemorrhage <1 Exertional 1 Brain tumor 0.1 Source: After J Olesen et al: The Headaches. Philadelphia, Lippincott, Williams & Wilkins, 2005. Anatomy and Physiology of Headache Pain usually occurs when peripheral nociceptors are stimulated in response to tissue injury, visceral distension, or other factors. In such situations, pain perception is a normal physiologic response mediated by a healthy nervous system. Pain can also result when pain-producing pathways of the peripheral or central nervous system (CNS) are damaged or activated inappropriately. Headache may originate from either or both mechanisms. Relatively few cranial structures are pain-producing; these include the scalp, middle meningeal artery, dural sinuses, falx cerebri, and proximal segments of the large pial arteries. The ventricular ependyma, choroid plexus, pial veins, and much of the brain parenchyma are not pain-producing. The key structures involved in primary headache appear to be the large intracranial vessels and dura mater the peripheral terminals of the trigeminal nerve that innervate these structures the caudal portion of the trigeminal nucleus, which extends into the dorsal horns of the upper cervical spinal cord and receives input from the first and second cervical nerve roots (the trigeminocervical complex) the pain modulatory systems in the brain that receive input from trigeminal nociceptors The innervation of the large intracranial vessels and dura mater by the trigeminal nerve is known as the trigeminovascular system. Autonomic symptoms, such as lacrimation and nasal congestion, are prominent in the trigeminal autonomic cephalalgias, including cluster headache and paroxysmal hemicrania, and may also be seen in migraine. . Migraine and other primary headache types are not "vascular headaches";. Clinical Evaluation of Acute, New-Onset Headache The patient who presents with a new, severe headache has a differential diagnosis that is quite different from the patient with recurrent headaches over many years. In new-onset and severe headache, the probability of finding a potentially serious cause is considerably greater than in recurrent headache. Patients with recent onset of pain require prompt evaluation and often treatment. Serious causes to be considered include meningitis, subarachnoid hemorrhage, epidural or subdural hematoma, glaucoma, and purulent sinusitis. When worrisome symptoms and signs are present (Table 15-2), rapid diagnosis and management is critical. Headache Symptoms that Suggest a Serious Underlying Disorder "Worst" headache ever First severe headache Subacute worsening over days or weeks Abnormal neurologic examination Fever or unexplained systemic signs Vomiting that precedes headache Pain induced by bending, lifting, cough Pain that disturbs sleep or presents immediately upon awakening Known systemic illness Onset after age 55 Pain associated with local tenderness, e.g., region of temporal artery A complete neurologic examination is an essential first step in the evaluation. In most cases, patients with an abnormal examination or a history of recent-onset headache should be evaluated by a CT or MRI study. . The psychological state of the patient should also be evaluated since a relationship exists between head pain and depression. Many patients in chronic daily pain cycles become depressed, although depression itself is rarely a cause of headache. Drugs with antidepressant actions are also effective in the prophylactic treatment of both tension-type headache and migraine. Underlying recurrent headache disorders may be activated by pain that follows otologic or endodontic surgical procedures. Thus, pain about the head as the result of diseased tissue or trauma may reawaken an otherwise quiescent migrainous syndrome. Treatment of the headache is largely ineffective until the cause of the primary problem is addressed. Serious underlying conditions that are associated with headache are described below. Brain tumor is a rare cause of headache and even less commonly a cause of severe pain. The vast majority of patients presenting with severe headache have a benign cause.

Secondary Headache The management of secondary headache focuses on diagnosis and treatment of the underlying condition. Meningitis Acute, severe headache with stiff neck and fever suggests meningitis. LP is mandatory. Often there is striking accentuation of pain with eye movement. Meningitis can be easily mistaken for migraine in that the cardinal symptoms of pounding headache, photophobia, nausea, and vomiting are present. Intracranial Hemorrhage Acute, severe headache with stiff neck but without fever suggests subarachnoid hemorrhage. A ruptured aneurysm, arteriovenous malformation, or intraparenchymal hemorrhage may also present with headache alone. Rarely, if the hemorrhage is small or below the foramen magnum, the head CT scan can be normal. Therefore, LP may be required to definitively diagnose subarachnoid hemorrhage.. Brain Tumor Approximately 30% of patients with brain tumors consider headache to be their chief complaint. The head pain is usually nondescript—an intermittent deep, dull aching of moderate intensity, which may worsen with exertion or change in position and may be associated with nausea and vomiting. This pattern of symptoms results from migraine far more often than from brain tumor. The headache of brain tumor disturbs sleep in about 10% of patients. Vomiting that precedes the appearance of headache by weeks is highly characteristic of posterior fossa brain tumors. A history of amenorrhea or galactorrhea should lead one to question whether a prolactin-secreting pituitary adenoma (or the polycystic ovary syndrome) is the source of headache. Headache arising de novo in a patient with known malignancy suggests either cerebral metastases or carcinomatous meningitis, or both. Head pain appearing abruptly after bending, lifting, or coughing can be due to a posterior fossa mass (or a Chiari malformation). . Temporal Arteritis Temporal (giant cell) arteritis is an inflammatory disorder of arteries that frequently involves the extracranial carotid circulation. It is a common disorder of the elderly; its annual incidence is 77 per 100,000 individuals ages 50 and older. The average age of onset is 70 years, and women account for 65% of cases. About half of patients with untreated temporal arteritis develop blindness due to involvement of the ophthalmic artery and its branches; indeed, the ischemic optic neuropathy induced by giant cell arteritis is the major cause of rapidly developing bilateral blindness in patients >60 years. Because treatment with glucocorticoids is effective in preventing this complication, prompt recognition of the disorder is important. Typical presenting symptoms include headache, polymyalgia rheumatica , jaw claudication, fever, and weight loss. Headache is the dominant symptom and often appears in association with malaise and muscle aches. Head pain may be unilateral or bilateral and is located temporally in 50% of patients but may involve any and all aspects of the cranium. Pain usually appears gradually over a few hours before peak intensity is reached; occasionally, it is explosive in onset. The quality of pain is only seldom throbbing; it is almost invariably described as dull and boring, with superimposed episodic stabbing pains similar to the sharp pains that appear in migraine. Most patients can recognize that the origin of their head pain is superficial, external to the skull, rather than originating deep within the cranium (the pain site for migraineurs). Scalp tenderness is present, often to a marked degree; brushing the hair or resting the head on a pillow may be impossible because of pain. Headache is usually worse at night and often aggravated by exposure to cold. Additional findings may include reddened, tender nodules or red streaking of the skin overlying the temporal arteries, and tenderness of the temporal or, less commonly, the occipital arteries. The erythrocyte sedimentation rate (ESR) is often, though not always, elevated; a normal ESR does not exclude giant cell arteritis. A temporal artery biopsy followed by treatment with prednisone 80 mg daily for the first 4–6 weeks should be initiated when clinical suspicion is high. The prevalence of migraine among the elderly is substantial, considerably higher than that of giant cell arteritis. Migraineurs often report amelioration of their headaches with prednisone; thus, caution must be used when interpreting the therapeutic response. Glaucoma Glaucoma may present with a prostrating headache associated with nausea and vomiting. The headache often starts with severe eye pain. On physical examination, the eye is often red with a fixed, moderately dilated pupil. .

Primary Headache Syndromes Primary headaches are disorders in which headache and associated features occur in the absence of any exogenous cause. The most common are migraine, tension-type headache, and cluster headache. Migraine Headache Migraine, the second most common cause of headache, afflicts approximately 15% of women and 6% of men. It is usually an episodic headache that is associated with certain features such as sensitivity to light, sound, or movement; nausea and vomiting often accompany the headache. A useful description of migraine is a benign and recurring syndrome of headache associated with other symptoms of neurologic dysfunction in varying admixtures. Migraine can often be recognized by its activators, referred to as triggers. Symptoms Accompanying Severe Migraine Attacks in 500 Patients Symptom Patients Affected, % Nausea 87 Photophobia 82 Lightheadedness 72 Scalp tenderness 65 Vomiting 56 Visual disturbances 36 Photopsia 26 Fortification spectra 10 Paresthesias 33 Vertigo 33 Alteration of consciousness 18 Syncope 10 Seizure 4 Confusional state 4 Diarrhea 16 Source: From NH Raskin, Headache, 2d ed. New York, Churchill Livingston, 1988; with permission. The brain of the migraineur is particularly sensitive to environmental and sensory stimuli; migraine-prone patients do not habituate easily to sensory stimuli. This sensitivity is amplified in females during the menstrual cycle. Headache can be initiated or amplified by various triggers, including glare, bright lights, sounds, or other afferent stimulation; hunger; excess stress; physical exertion; stormy weather or barometric pressure changes; hormonal fluctuations during menses; lack of or excess sleep; and alcohol or other chemical stimulation. Knowledge of a patient's susceptibility to specific triggers can be useful in management strategies involving lifestyle adjustments. Pathogenesis The sensory sensitivity that is characteristic of migraine is probably due to dysfunction of monoaminergic sensory control systems located in the brainstem and thalamus (Fig. 15-1). Figure 15-1 Brainstem pathways that modulate sensory input. The key pathway for pain in migraine is the trigeminovascular input from the meningeal vessels, which passes through the trigeminal ganglion and synapses on second-order neurons in the trigeminocervical complex. These neurons in turn project in the quintothalamic tract and, after decussating in the brainstem, synapse on neurons in the thalamus. Important modulation of the trigeminovascular nociceptive input comes from the dorsal raphe nucleus, locus coeruleus, and nucleus raphe magnus. Diagnosis and Clinical Features Diagnostic criteria for migraine headache are listed in Table 15-4. A high index of suspicion is required to diagnose migraine: the migraine aura, consisting of visual disturbances with flashing lights or zigzag lines moving across the visual field or of other neurologic symptoms, is reported in only 20–25% of patients. A headache diary can often be helpful in making the diagnosis; this is also helpful in assessing disability and the frequency of treatment for acute attacks. Patients with episodes of migraine that occur daily or near-daily are considered to have chronic migraine (see "Chronic Daily Headache," below). Migraine must be differentiated from tension-type headache (discussed below), the most common primary headache syndrome seen in clinical practice. Migraine at its most basic level is headache with associated features, and tension-type headache is headache that is featureless. Most patients with disabling headache probably have migraine. Simplified Diagnostic Criteria for Migraine Repeated attacks of headache lasting 4–72 h in patients with a normal physical examination, no other reasonable cause for the headache, and: At least 2 of the following features: Plus at least 1 of the following features: Unilateral pain Nausea/vomiting Throbbing pain Photophobia and phonophobia Aggravation by movement Moderate or severe intensity Source: Adapted from the International Headache Society Classification (Headache Classification Committee of the International Headache Society, 2004). Table 15-7 Preventive Treatments in Migrainea Drug Dose Selected Side Effects Pizotifenb 0.5–2 mg qd Weight gain Drowsiness Beta blocker Propranolol 40–120 mg bid Reduced energy Tiredness Postural symptoms Contraindicated in asthma Tricyclics Amitriptyline 10–75 mg at night Drowsiness Dothiepin 25–75 mg at night Nortriptyline 25–75 mg at night Note: Some patients may only need a total dose of 10 mg, although generally 1–1.5 mg/kg body weight is required Anticonvulsants Topiramate 25–200 mg/d Paresthesias Cognitive symptoms Weight loss Glaucoma Caution with nephrolithiasis Valproate 400–600 mg bid Drowsiness Weight gain Tremor Hair loss Fetal abnormalities Hematologic or liver abnormalities Gabapentin 900–3600 mg qd Dizziness Sedation Serotonergic drugs Methysergide 1–4 mg qd Drowsiness Leg cramps Hair loss Retroperitoneal fibrosis (1-month drug holiday is required every 6 months) Flunarizineb 5–15 mg qd Drowsiness Weight gain Depression Parkinsonism No convincing evidence from controlled trials Verapamil Controlled trials demonstrate no effect Nimodipine Clonidine SSRIs: fluoxetine aCommonly used preventives are listed with reasonable doses and common side effects. Not all listed medicines are approved by the FDA; local regulations and guidelines should be consulted. bNot available in the United States. Drug Trade Name Dosage Simple Analgesics Acetaminophen, aspirin, caffeine Excedrin Migraine Two tablets or caplets q6h (max 8 per day) NSAIDs Ibuprofen Advil, Motrin, Nuprin, generic 400 mg PO q3–4h Tolfenamic acid Clotam Rapid 200 mg PO. May repeat x 1 after 1–2 h 5-HT1 Agonists Oral Ergotamine Ergomar One 2 mg sublingual tablet at onset and q1/2h (max 3 per day, 5 per week) Ergotamine 1 mg, caffeine 100 mg Ercaf, Wigraine One or two tablets at onset, then one tablet q1/2h (max 6 per day, 10 per week) Rizatriptan Maxalt Maxalt-MLT 5–10 mg tablet at onset; may repeat after 2 h (max 30 mg/d) Sumatriptan Imitrex 50–100 mg tablet at onset; may repeat after 2 h (max 200 mg/d) Nasal Dihydroergotamine Migranal Nasal Spray Prior to nasal spray, the pump must be primed 4 times; 1 spray (0.5 mg) is administered, followed in 15 min by a second spray Sumatriptan Imitrex Nasal Spray 5–20 mg intranasal spray as 4 sprays of 5 mg or a single 20 mg spray (may repeat once after 2 h, not to exceed a dose of 40 mg/d) Zolmitriptan Zomig 5 mg intranasal spray as one spray (may repeat once after 2 h, not to exceed a dose of 10 mg/d) Parenteral Dihydroergotamine DHE-45 1 mg IV, IM, or SC at onset and q1h (max 3 mg/d, 6 mg per week) Sumatriptan Imitrex Injection 6 mg SC at onset (may repeat once after 1 h for max of 2 doses in 24 h) Dopamine Antagonists Oral Metoclopramide Reglan,a generica 5–10 mg/d Prochlorperazine Compazine,a generica 1–25 mg/d Parenteral Chlorpromazine Generica 0.1 mg/kg IV at 2 mg/min; max 35 mg/d Metoclopramide Reglan,a generic 10 mg IV Prochlorperazine Compazine,a generica 10 mg IV Other Oral Acetaminophen, 325 mg, plus dichloralphenazone, 100 mg, plus isometheptene, 65 mg Midrin, Duradrin, generic Two capsules at onset followed by 1 capsule q1h (max 5 capsules) Nasal Butorphanol Stadola 1 mg (1 spray in 1 nostril), may repeat if necessary in 1–2 h aNot all drugs are specifTension-Type Headache Tension Type Headache Clinical Features The term tension-type headache (TTH) is commonly used to describe a chronic head-pain syndrome characterized by bilateral tight, bandlike discomfort. The pain typically builds slowly, fluctuates in severity, and may persist more or less continuously for many days. The headache may be episodic or chronic (present >15 days per month). A useful clinical approach is to diagnose TTH in patients whose headaches are completely without accompanying features such as nausea, vomiting, photophobia, phonophobia, osmophobia, throbbing, and aggravation with movement. Such an approach neatly separates migraine, which has one or more of these features and is the main differential diagnosis, from TTH. However, the International Headache Society's definition of TTH allows an admixture of nausea, photophobia, or phonophobia in various combinations, illustrating the difficulties in distinguishing these two clinical entities. Patients whose headaches fit the TTH phenotype and who have migraine at other times, along with a family history of migraine, migrainous illnesses of childhood, or typical migraine triggers to their migraine attacks, may be biologically different from those who have TTH headache with none of the features. Pathophysiology The pathophysiology of TTH is incompletely understood. It seems likely that TTH is due to a primary disorder of CNS pain modulation alone, unlike migraine, which involves a more generalized disturbance of sensory modulation. Data suggest a genetic contribution to TTH, but this may not be a valid finding: given the current diagnostic criteria, the studies undoubtedly included many migraine patients. The name tension-type headache implies that pain is a product of nervous tension, but there is no clear evidence for tension as an etiology. Muscle contraction has been considered to be a feature that distinguishes TTH from migraine, but there appear to be no differences in contraction between the two headache types. Tension-Type Headache: Treatment The pain of TTH can generally be managed with simple analgesics such as acetaminophen, aspirin, or NSAIDs. Behavioral approaches including relaxation can also be effective. Clinical studies have demonstrated that triptans in pure TTH are not helpful, although triptans are effective in TTH when the patient also has migraineically indicated by the FDA for migraine. Local regulations and guidelines should be consulted. For chronic TTH amitriptiline is the only proven treatment. Trigeminal Autonomic Cephalalgias, Including Cluster Headache The trigeminal autonomic cephalalgias (TACs) are a group of primary headaches that includes cluster headache, paroxysmal hemicrania, and SUNCT (short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing). TACs are characterized by relatively short-lasting attacks of head pain associated with cranial autonomic symptoms, such as lacrimation, conjunctival injection, or nasal congestion (Table 15-8). Pain is usually severe and may occur more than once a day. Because of the associated nasal congestion or rhinorrhea, patients are often misdiagnosed with "sinus headache" and treated with decongestants, which are ineffective. Table 15-8 Clinical Features of the Trigeminal Autonomic Cephalalgias Cluster Headache Paroxysmal Hemicrania SUNCT Gender M>F F=M F~M Pain Type Stabbing, boring Throbbing, boring, stabbing Burning, stabbing, sharp Severity Excruciating Excruciating Severe to excruciating Site Orbit, temple Orbit, temple Periorbital Attack frequency 1/alternate day– 8/d 1–40/d (>5/d for more than half the time) 3–200/d Duration of attack 15–180 min 2–30 min 5–240 s Autonomic features Yes Yes Yes (prominent conjunctival injection and lacrimation)a Migrainous featuresb Yes Yes Yes Alcohol trigger Yes No No Cutaneous triggers No No Yes Indomethacin effect — Yesc — Abortive treatment Sumatriptan injection or nasal spray Oxygen No effective treatment Lidocaine (IV) Prophylactic treatment Verapamil Methysergide Lithium Indomethacin Lamotrigine Topiramate Gabapentin aIf conjunctival injection and tearing not present, consider SUNA. These are the common varieties of headache we come across in our daily life....