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Diagnosis of Basilar artery migraine

Basilar artery migraine Diagnosis: Book Excerpts

Diagnostic Tests for Basilar artery migraine: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Basilar artery migraine.


HEADACHE: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is there a history of drug, caffeine, or alcohol ingestion? The hangover headache is well known and should not present a problem in diagnosis. Caffeine withdrawal headaches are also common because of the large amount of caffeine consumed in coffee, various soft drinks, and chocolate. Drugs that may induce headache include the nonsteroidal anti-inflammatory drugs such as indomethacin (Indocin®) and the anti-hypertensives such as clonidine, aspirin, quinidine, and bromides.
  2. Is there a history of trauma? Trauma may cause concussion and postconcussion headaches, intracranial neoplasms such as subdural hematoma, and cervical sprain, all of which can induce headaches.
  3. Is the headache acute or chronic? An acute onset of a headache can be a serious problem. It should be taken seriously because it may mean a subarachnoid hemorrhage or meningitis. This can be easily confirmed by checking for nuchal rigidity. Whenever there is an acute onset of a headache this must be done. Chronic headaches, on the other hand, are most likely due either to migraine if they occur in exacerbations or remissions, or to tension headaches if they are fairly constant, mild, and chronic. The headache of a brain tumor is rarely severe and is rarely the presenting symptom of a brain tumor. Headaches that occur in clusters almost daily for 6 to 8 weeks with interruptions of several months must make one consider cluster headaches. Unilateral headaches in the elderly with acute onset should make one think of temporal arteritis.
  4. Is there nuchal rigidity? The presence of nuchal rigidity should make one think of a subarachnoid hemorrhage or meningitis, but it may also be due to cerebral hemorrhage or cerebral abscess.
  5. Is there fever? If the headache is associated with fever, the possibility of acute sinusitis should be considered, and the sinuses should be transilluminated. Other sources for the fever should be looked for, and meningitis or encephalitis should be considered.
  6. Is there papilledema or are there focal neurologic signs? With acute headache and focal neurologic signs and/or papilledema, one should consider cerebral abscess or cerebral hemorrhage. With a chronic headache and papilledema or focal neurologic signs, one should consider a space-occupying lesion such as a primary brain tumor or metastatic neoplasm.
  7. Do the sinuses transilluminate well? A sinus transilluminator should be in the armamentarium of every physician who expects to diagnose headache. If the sinuses fail to transilluminate, one should consider acute sinusitis as the diagnosis.
  8. Is there tenderness of the superficial temporal artery? The presence of a tender superficial temporal artery should make one think of temporal arteritis, particularly in the elderly, but it may also be related to a long-standing migraine attack.
  9. Is the headache relieved by superficial temporal artery compression? Relief of the headache on superficial temporal artery compression should suggest classical or common migraine. If one can relieve the headache by compression of the occipital artery, occipital migraine should be considered. When there is no relief on compression of the superficial temporal artery, one should consider tension headaches, occipital neuralgia, cervical spondylosis, and cluster headaches as the cause.

DIAGNOSTIC WORKUP

Routine diagnostic tests include a CBC to rule out severe anemia, a sedimentation rate to rule out temporal arteritis, a chemistry panel to rule out liver and kidney disease, a VDRL test to rule out central nervous system syphilis, an x-ray of the sinuses to rule out sinusitis, and an x-ray of the cervical spine to exclude cervical spondylosis. A chest x-ray should also be done to rule out the possibility of metastatic neoplasm. A tonometry study may be done if glaucoma is suspected.

If there are focal neurologic signs, referral should be made to a neurologist or neurosurgeon as soon as possible. If one is not readily available, a CT scan or MRI may be done, the CT scan being the preferred procedure if the expense is a consideration.

If there is nuchal rigidity, a CT scan should be done to rule out a space-occupying lesion before proceeding with a spinal tap. If the CT scan is negative, a spinal tap can be done, and this will ascertain whether there is intracranial bleeding or meningitis. It is usually best to refer the patient to a neurologist or neurosurgeon if there is nuchal rigidity.

If the headaches are chronic and episodic, and there are no focal neurologic signs, papilledema, or nuchal rigidity, an imaging study can be postponed for a while until the response to treatment is evaluated. However, if the response to treatment is poor, one should not hesitate to order a CT scan or MRI.

Difficult cases of headache should also be studied with 24-hr blood pressure monitoring, a 24-hr urine for catecholamines, and lumbar puncture to diagnose central nervous system lues. Histamine phosphate 0.5 cc subcutaneously may help diagnose cluster headaches. Response to beta-blockers may help diagnose migraine. Cerebral angiography may be necessary to diagnose aneurysms and arteriovenous malformations. Patients with chronic headache unresponsive to therapy should be referred to a psychiatrist.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

SYNCOPE: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Are there convulsive movements or incontinence? The presence of convulsive movements should suggest convulsions, and the differential diagnosis of this is discussed on page 88 . Convulsive movements can occur with other forms of syncope, however.
  2. Is the pulse slow or absent? The presence of a slow or absent pulse would suggest heart block, vasovagal syncope, and carotid sinus syncope.
  3. Is the pulse rate normal? The presence of a normal pulse rate would suggest anemia, aortic stenosis, aortic insufficiency, and cyanotic congenital heart disease.
  4. Is the pulse rate rapid? The presence of a rapid pulse would suggest the various types of ventricular and supraventricular tachycardias, including auricular fibrillation and flutter, and it should also suggest heat exhaustion or heat stroke.
  5. If the pulse is rapid, is it regular? The presence of a rapid regular pulse should suggest supraventricular or ventricular tachycardia, heat exhaustion, or heat stroke.
  6. Is there a heart murmur? The presence of a heart murmur should suggest aortic stenosis, aortic insufficiency, and cyanotic congenital heart disease.
  7. Is there pallor? The presence of pallor should suggest shock or severe anemia and acute bleeding.
  8. Are there focal neurologic signs? The presence of focal neurologic signs should suggest cerebral vascular insufficiency, hypoglycemia, and transient ischemic attacks.

DIAGNOSTIC WORKUP

The diagnostic workup includes a CBC, sedimentation rate, urinalysis, chemistry panel, VDRL test, thyroid profile, glucose tolerance test, EKG, and chest x-ray. Several blood pressure recordings in the recumbent and upright positions should be made. If hypoglycemia is suspected, a 72-hr fast and a tolbutamide tolerance test should be done. The drug history should always be reviewed. A toxicology screen may be helpful.

Most cases will require 24-hr Holter monitoring or event Holter monitoring. In addition, other cardiovascular studies, such as echocardiography and His' bundle studies, may need to be done. Exercise tolerance testing is useful when the syncope seems to be exercise induced. An upright-tilt test is helpful when vasodepressor syncope is suspected, especially when combined with isoproterenol infusion. Signal-averaged EKG can be useful if a ventricular arrhythmia is suspected. If transient ischemic attacks are suspected, a carotid scan and cerebral angiography may be necessary. If the syncopal attacks are thought to be due to epilepsy, a wake-and-sleep EEG may need to be done. A CT scan or MRI of the brain may need to be done.

A cardiologist or neurologist should be consulted before ordering expensive diagnostic tests. A psychiatrist may also need to be consulted.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

Aura: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Epilepsy
    –Recurrent seizures
    –Strong family history
  • Migraine with aura
    –Usually visual aura (e.g., scotoma, flashing lights) lasting less than 60 minutes
    –Usually fully reversible with rare migrainous infarction (like CVA)
    –Migraine headache follows aura within 60 minutes and lasts 4–72 hours; however, aura may occur without headache
    • Partial seizure
      –60% of patients with focal seizures have an accompanying aura
      –Aura symptoms are associated with the brain area where they originate (e.g., occipital lobe seizure results in seeing lights)
      –Simple partial seizures result in focal tonic-clonic motor activity without loss of consciousness
      –Complex partial seizures progress to decreased consciousness and unresponsiveness
    • Tonic-clonic (grand mal seizure) seizures result in an abrupt loss of consciousness followed by stiffness (tonic); the patient then starts jerking (clonic) for an additional 2–3 minutes; rare aura
    • Pituitary adenoma or other underlying pathology that predisposes to migraines, seizures, or altered sensations (taste, smell)
    • Hallucinations (not actually an aura)
      • Physiologic nonepileptic seizures
        –Usually due to an underlying physiologic cause (e.g., fever, hypoglycemia, hypo- or hyperthyroidism, renal failure, cerebral anoxia)
    • Absence seizures (petit mal seizure) only rarely have an aura

    Workup and Diagnosis

    • History is very important
      –Type of aura (any of five senses)
      –Loss of consciousness
      –Associated activities and triggers (e.g., stress, medications, exertion, trauma, foods)
      –Postaura symptoms (e.g., headache, loss of consciousness, seizure)
      –History or family history of seizures or migraines
      –Review past medical history for head injury, stroke, dementia, intracranial infection, and alcohol or drug abuse
      –Full head, neck, and neurologic exam (look for one-sided features that suggest pathology on opposite side of brain)
      –Examine for trauma following loss of consciousness
    • Initial tests may include glucose, electrolytes, calcium, magnesium, CBC, BUN/creatinine, and toxicology screen
      • EEG may be indicated if seizure activity is suspected
        (provocative EEG with triggers gives higher yield)
        –Normal EEG does not rule out epilepsy
        –May be abnormal in migraines
      • MRI to rule out cerebral pathology
      • CT if physiologic seizure or trauma is involved (not indicated in patients with migraine and normal neurologic exam unless pattern of migraine has changed)

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Headache: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Tension-type headache
    –Most common cause of headache
    –Diffuse, bilateral, band-like pain
    –Lasts for hours to days
    –May occur on a fairly regular basis
  • Migraine headache
    –Throbbing unilateral or bilateral pain
    –May last for days
    –May have preceding aura (flashing light)
    –Triggers include foods, drugs, or stress
  • Meningitis
    –May present with fever, photophobia, neck stiffness, nausea/vomiting, papilledema
    –Brudzinski's sign: Neck pain upon passive flexion of neck
    –Kernig's sign: Neck pain and involuntary flexion upon passive extension of knee with hips flexed
  • Head trauma
  • Medications
  • Carbon monoxide exposure
  • Sinusitis
  • Temporomandibular joint syndrome or dental pain
  • Withdrawal from alcohol, barbiturates, caffeine, or other substance
  • Temporal arteritis
    –Pain/tenderness over temporal area/jaw
    –Occurs uniquely in patients over 50
    –Blindness may occur
  • Mass lesions (e.g., tumor, hematoma)
    –Daily, progressive headache
    –May awaken from sleep
    –Focal neurologic signs
  • Subarachnoid hemorrhage
    –Sudden onset of “worst headache of my life”
    –Neck stiffness
    –Loss of consciousness
  • Cluster headache
    –Severe, unilateral pain
    –Lasts minutes to hours
    –Occurs daily for months, then remits for months or even years
  • Glaucoma
    –Retro-orbital pain
  • Chronic daily headache or rebound headache (e.g., secondary to chronic analgesic use)
  • Benign intracranial hypertension

Workup and Diagnosis

  • History and physical exam often make the diagnosis
    –History should focus on onset, duration, frequency, possible triggers, severity, quality (e.g., throbbing, band-like), accompanying symptoms (e.g., aura, photophobia, visual changes, nausea/vomiting, lacrimation, nasal congestion), constitutional symptoms (e.g., weight loss, fever), medications, and dietary history
    –Is this first and/or worst headache of life?
    –Exam should include a complete neurologic exam, visual/retinal exam, head/neck, and gait exam
  • Possible serious etiologies and need for further workup are suggested by the following red flags: Constitutional symptoms, new headache in a patient over 50, sudden onset, awakening from sleep, mental status changes, focal neurologic signs, visual/motor/balance disturbance, papilledema
  • CT will identify hemorrhage and mass lesions and rule out increased intracranial pressure
  • MRI will identify posterior fossa tumors
  • Lumbar puncture is indicated if CT is normal but still suspect hemorrhage, infection, or tumor
  • Serologies for bacterial, viral, and other causes of meningitis or encephalitis
  • Elevated ESR suggests temporal arteritis or infection
  • Carboxyhemoglobin measurement if history suggests carbon monoxide poisoning

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Syncope: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Vasovagal episode
    –Most common cause of syncope
    –May be triggered by heat, fatigue, stress, hunger, alcohol, and severe pain
    –Associated with diaphoresis, weakness, blurry vision, lightheadedness
    –Almost always benign
  • Orthostatic hypotension
    –Fall in blood pressure upon standing, due to failure of vasoconstrictor reflexes
    –Precipitated by sudden standing from recumbent position
    –Often associated with antihypertensive medications (diuretics, vasodilators, α - or β-blockers) and dehydration/hypovolemia
    –May occur with autonomic disorders (e.g., Shy-Drager syndrome)
    • Situational syncope
      –Increased intrathoracic pressure (e.g., cough, micturition, defecation) leads to decreased venous return and resulting diminished blood flow to the brain
    • Cardiac arrhythmias
      –Very slow (<30 bpm) or fast (>180 bpm) heart rates may result in decreased cardiac output and resulting diminished blood flow to the brain
  • Valvular disease
    –Most commonly due to aortic stenosis
  • Myocardial disease
    • Cerebrovascular disease
      –Usually due to carotid or vertebrobasilar atherosclerosis
  • Hypoglycemia
  • Anemia
  • Seizure
  • Anxiety attack
  • Migraine
  • Medications (e.g., anticholinergics)
  • CVA
  • Hemorrhage
  • Trauma

Workup and Diagnosis

  • History and physical exam will often suggest the underlying etiology
    –Note pre- and postsyncopal symptoms (e.g., chest pain, dizziness, lightheadedness, nausea/vomiting, headache, diaphoresis, blurry vision, blindness)
    –Full HEENT, neurologic, and cardiovascular exam
    –Examine for trauma following syncope
    –Record BP in supine, sitting, standing, and in both arms
    –Strategically attempt to reproduce syncope by Valsalva maneuver (e.g., coughing, deep breathing for 2–3 min)
  • Initial labs should include CBC, electrolytes, calcium, magnesium, glucose, toxicology screens, and ECG
  • Further cardiovascular testing may include cardiac enzymes if ischemia is suspected, 24-hour Holter monitor, echocardiogram, stress testing, and/or invasive cardiac monitoring
  • Head CT to rule out cerebral disease
  • Doppler ultrasound of carotids if bruit is heard
  • EEG may be useful if seizure disorder is suspected
  • Tilt table test may induce vasovagal episode
  • Plasma aldosterone/mineralocorticoid levels to evaluate for hypovolemia due to adrenocortical insufficiency
>

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Headache: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

  • Migraine
    –Recurring headache with throbbing, pulsating pain; nausea and vomiting; photophobia, phonophobia
    –Family history of migraine
    –Improvement with rest/sleep
    –Without aura (common migraine) 85%
    –With aura (classic migraine) 15%
    –Frequently bilateral pain in children
    –Aura usually develops over 5 minutes and is most commonly visual
    –Migraine is an episodic disorder
    –Chronic daily headache is not migraine
    • Tension headache
      • Pseudotumor cerebri
        –Elevated ICP with no masses or abnormalities in CSF or labs
      • Cluster headache
        –Unilateral nonthrobbing, periorbital pain
        –May have ipsilateral conjectival injection, lacrimation, rhinorrhea
    • Subarachnoid hemorrhage
      –Sudden paroxysmal headache
      –Meningeal signs
      –An emergency requiring CT and LP
    • Increased intracranial pressure
      –Tumor, abscess, hydrocephalus, hemorrhage
    • Sinusitis, otitis
    • Dental disease
    • Systemic infection
    • TMJ disease
    • Postconcussive syndrome
    • Trigeminal neuralgia
    • Mitochondrial disorders
    • Venous sinus thrombosis
    • Meningitis/encephalitis
    • CSF leak, post-lumbar puncture
    • Hypertensive crisis
    • Trauma
    • Arteriovenous malformation
    • Stroke
    • Toxins and medication
      –Nitrites, cocaine, interferon, CO
    • Fever
    • Anemia

    Workup and Diagnosis

      • History
        –Duration (recurrent, progressive), frequency
        –Time of onset and duration
        –Location and nature of pain, warning (aura)
        –Factors that alleviate or exacerbate symptoms (e.g., stress)
        –Nausea, vomiting, photophobia, phonophobia
        –Family history, response to treatment
    • Physical exam
      –Vital signs (temperature, blood pressure)
      –Height, weight, head circumference
      –Funduscopy (to rule out papilledema)
    • Neuroimaging (CT, MRI) is required for certain symptoms
      –Short history of headache (<6 months) or age <5–6 years
      –Worsening headaches, no response to treatment
      –Deterioration in cognitive or motor function
      –Short stature, macrocephaly
      –Awakening at night or early morning
      –Repeated morning vomiting
      –Exacerbation by position change or cough
      –Focal neurologic symptoms during headache
      –Cluster headache in prepubertal children and adolescent girls
      –Systemic symptoms: Fatigue, weight loss
      –Abnormal neurological exam
      • Lumbar puncture with opening pressure
        –Subarachnoid hemorrhage, pseudotumor, or meningitis
      >>

    » READ BOOK EXCERPT ONLINE »

    Source: In A Page: Pediatric Signs and Symptoms, 2007

    Umbilicus – Single Umbilical Artery: Differential Diagnosis
    (In A Page: Pediatric Signs and Symptoms)

    • Developmental agenesis or hypoplasia
      –No clear sex ratio
      –Males more likely to have associated malformations
      –Increased incidence in twins, either mono- or dizygotic
      –Increased incidence of placental anomalies
      –More common in low birth weight infants
      –More common in premature infants
    • Associated maternal factors
      –Maternal diabetes
      –Maternal epilepsy
      –Toxemia
    • Intrauterine thrombosis of other umbilical artery
    • Malformations are associated with SUA in 45% of cases
      –Genitourinary (33%): Renal agenesis, dysgenesis, hypoplasia; ambiguous genitalia
      –Musculoskeletal (37%): Clubfoot, vertebral anomalies
      –Cardiovascular (30%): Patent ductus arteriosus, ventricular septal defect, dextrocardia
      –Gastrointestinal (28%): Imperforate anus, tracheoesophageal fistula
      –Respiratory (9%): Pulmonary hypoplasia (malformations due to disruption of blood flow), sirenomelia
    • Chromosomal anomalies
      –Trisomy 18

    Workup and Diagnosis

    • History
      –Prenatal tests such as amniocentesis with karyotype
      –Twinning
      • Physical exam
        –Dysmorphic facial features
        –Anomalies with genitourinary, gastrointestinal, cardiac, musculoskeletal organ systems
        –Neurologic signs associated with stroke (e.g., seizures)
    • Level II prenatal ultrasound with Doppler examination of umbilical cord
      • Examination of placenta and cord at delivery
        –Examine closer to umbilical end of cord since vessels may merge close to placental insertion
    • Karyotype
    • Genetics consultation
    • Thrombophilia evaluation
      –Factor V Leiden or antithrombin III deficiency
      –Anticardiolipin or lupus anticoagulant

    » READ BOOK EXCERPT ONLINE »

    Source: In A Page: Pediatric Signs and Symptoms, 2007

    Syncope: Differential Diagnosis
    (In A Page: Pediatric Signs and Symptoms)

    • Vasovagal
      –Most common etiology (more than 50%)
      –Also known as neurocardiogenic or vasodepressor syncope
      –Typical in adolescents; greater in females
      –Occurs after prolonged standing in a warm place; with emotional upset, pain, hunger, the sight of blood; crowded places
    • Postural/orthostatic hypotension
      –Occurs when standing up quickly
    • Micturation syncope (a rare form)
    • Breath-holding spells
      –Usually at ages 1–5 years
      –Two types: Cyanotic (80%) vs pale (20%)
      –Cyanotic spells start with crying
      –Provoked by anger, frustration, or pain, or used as an attention-getting behavior
      –May have generalized clonic jerks
      • Cardiac etiologies (less common)
        –Arrhythmias
        –Supraventricular tachycardia is the most common cause
        –Long QT syndrome (QTc >0.44 seconds): Causes ventricular arrhythmias, Romano-Ward (autosomal dominant), Jervell and Lange-Nielsen (autosomal recessive with deafness)
        –Medications (e.g., cisapride)
        –Sinus node dysfunction and atrioventricular block may lead to bradyarrhythmias
        –Post-op congenital lesions and dilated cardiomyopathy lead to arrhythmias
        –Structural cardiac disease
        –Severe obstructive lesions (e.g., hypertrophic obstructive cardiomyopathy, aortic stenosis, pulmonic stenosis, atrial myxomas, and pulmonary hypertension)
      • Hysterical fainting
      • Migraine
      • Hyperventilation
      • Pregnancy
      • Anemia or hypovolemia
      • Hypoglycemia
      • Carbon monoxide poisoning
      • Medications and drugs of abuse
      • Electrolyte abnormalities
      • Intracranial hypertension
      • Epilepsy may mimic syncope
      • Adrenal insufficiency

      Workup and Diagnosis

      • History: Most important aspect to guide diagnostic workup
        –Vasovagal syncope: Prodromal symptoms (e.g., cold, clammy skin; pallor; nausea; blurry vision; yawning; dizziness; lightheadedness; palpitations; hyperventilation)
        –Duration: Vasovagal syncope is short (seconds to minutes)
        –Inciting situations
        –Lightheadedness: In orthostatic hypotension
        –Syncope at rest or recumbent in seizure or arrhythmia; syncope without prodrome or with exercise/exertion in cardiac etiology
        –Auras in migraine headaches
        –Seizures may have incontinent or post-ictal state or generalized tonic-clonic movements
        –Family history: Sudden or unexplained deaths, cardiac abnormalities, seizures, or deafness
      • Physical exam
        –Orthostatic blood pressures and pulse
        –Perform a thorough cardiac and neurologic exam
      • Extensive laboratory workup is not usually needed
        –Most clinicians would do an ECG
        –Tilt-table testing to diagnose vasovagal syncope is controversial as it is not very reproducible
        –Labs might include CBC, glucose, electrolytes, drug screen, carboxyhemoglobin, EEG, or head CT as guided by history; if cardiac abnormalities are suspected, may get a chest X-ray, Holter monitoring, or exercise testing

    » READ BOOK EXCERPT ONLINE »

    Source: In A Page: Pediatric Signs and Symptoms, 2007

    HEADACHE: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The patient presenting with a history of headaches is an exciting diagnostic challenge. If one approaches the challenge simply on the basis of what is common, the patient most likely has migraine or muscle traction headache. But, wait a minute! Shouldn’t we look for serious conditions such as brain tumor, meningitis, or subarachnoid hemorrhage to avoid a serious mistake and a malpractice suit? First, check for nuchal rigidity to rule out meningitis and subarachnoid headache. Next, do a careful neurologic examination to rule out a brain tumor or other space-occupying lesion. These steps are particularly important in a patient is experiencing his or her first serious headache. If there is nuchal rigidity or focal neurologic signs, it is wise to immediately refer the patient to a neurologist or neurosurgeon for further workup and possible hospitalization. The specialist will probably order a CT scan of the brain and follow that with a spinal tap if a subarachnoid hemorrhage or meningitis is suspected. It is clear that a CT scan should be done prior to a spinal tap if there are focal neurologic signs or papilledema. One other condition that must be considered in acute headache particularly in the elderly is temporal arteritis. A sedimentation rate will usually be positive but a neurology consult is axiomatic so that steroids can be started immediately.

    In the patient with chronic or recurring headaches and no neurologic findings, it is wise to see the patient during the attack. Migraine and histamine headaches can be diagnosed by the response to sumatriptan by mouth or injection. If the headaches are due to chronic allergic or infectious rhinitis, relief can be had by spraying the turbinates with phenylephrine. Muscle traction headaches will often be relieved by occipital nerve blocks supporting the diagnosis. Compression of the superficial temporal artery will often relieve migraine temporarily supporting that diagnosis. Compression of the jugular veins will often give relief to post spinal tap headaches.

    If the patient is seen between headaches, certain prophylactic measures may help establish the diagnosis. For migraine, β-blockers may be prescribed and if the headaches are prevented, there is good support for the diagnosis. A course of corticosteroids may be initiated in patients with histamine (cluster) headaches to help establish the diagnosis. Muscle relaxants and/or tricyclic drugs may be given to help diagnose muscle contraction headaches.

    The diagnostic workup of chronic headaches might include a CT scan of the brain, x-rays of the sinuses, x-rays of the cervical spine and routine blood work. Certainly if headache persists after careful follow up, these need to be done.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    SYNCOPE: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    Clinical differentiation of the various forms of syncope is made by combinations of symptoms. Thus, syncope with marked sweating and tachycardia is more likely due to hypoglycemia. Syncope with sweating and bradycardia is more likely due to vasovagal syncope. Focal neurologic signs during the attack suggest transient cerebral ischemia (TIA) and prompt a search for sources of emboli or thrombosis (sickle cell disease, polycythemia, or macroglobulinemia). A family history of syncope suggests migraine, epilepsy, or vasovagal attacks. Epilepsy is a strong possibility in the young, whereas heart block is more likely in the aged. Consequently, an EEG and Holter monitoring are useful in the workup.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    Aura: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    Obtain a thorough history of the patient’s headaches or seizure history, asking him to describe any sensory or motor phenomena that precede each headache or seizure. Find out how long each headache or seizure typically lasts. Does anything make it worse, such as bright lights, noise, or caffeine? Does anything make it better? Ask the patient about drugs he takes for pain relief.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Headache: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    If the patient reports a headache, ask him to describe its characteristics and location. How often does he get a headache? How long does a typical headache last? Try to identify precipitating factors, such as certain foods or exposure to bright lights. Ask what helps to relieve the headache. Is the patient under stress? Has he had trouble sleeping?

    Take a drug and alcohol history, and ask about head trauma within the past 4 weeks. Has the patient recently experienced nausea, vomiting, photophobia, or visual changes? Does he feel drowsy, confused, or dizzy? Has he recently developed seizures or does he have a history of seizures?

    Begin the physical examination by evaluating the patient’s level of consciousness (LOC). Then check his vital signs. Be alert for signs of increased ICP — a widened pulse pressure, bradycardia, an altered respiratory pattern, and increased blood pressure. Check pupil size and response to light, and note any neck stiffness.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Syncope: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur?

    Next, take the patient’s vital signs and examine him for any injuries that may have occurred during his fall.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Headache: Diagnosis
    (Professional Guide to Diseases (Eighth Edition))

    Diagnosis requires a history of recurrent headaches and physical examination of the head and neck. Such examination includes percussion, auscultation for bruits, inspection for signs of infection, and palpation for defects, crepitus, or tender spots (especially after trauma). Firm diagnosis also requires a complete neurologic examination, assessment for other systemic diseases — such as hypertension — and a psychosocial evaluation, when such factors are suspected.

    Diagnostic tests include cervical spine and sinus X-rays, EEG, computed tomography scan — performed before lumbar puncture to rule out increased intracranial pressure (ICP) — or magnetic resonance imaging. A lumbar puncture isn’t done if there’s evidence of increased ICP or if a brain tumor is suspected because rapidly reducing pressure by removing spinal fluid can cause brain herniation.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Diseases (Eighth Edition), 2005

    Premenstrual syndrome: Diagnosis
    (Professional Guide to Diseases (Eighth Edition))

    The patient history shows typical symptoms related to the menstrual cycle. To help ensure an accurate history, the patient may be asked to record menstrual symptoms and body temperature on a calendar for 2 to 3 months prior to diagnosis. Estrogen and progesterone blood levels may be evaluated to help rule out hormonal imbalance. A psychological evaluation is also recommended to rule out or detect an underlying psychiatric disorder.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Diseases (Eighth Edition), 2005

    Aura: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    After providing emergency care, obtain a thorough history of the patient’s headaches or seizures, asking him to describe any sensory or motor phenomena that precede each headache or seizure. Find out how long each headache or seizure typically lasts. Does anything make it worse, such as bright lights, noise, or caffeine? Does anything make it better? Ask the patient about drugs he takes for pain relief.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Headache: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    If the patient reports a headache, ask him to describe its characteristics and location. How often does he get a headache? How long does a typical headache last? Try to identify precipitating factors, such as eating certain foods or exposure to bright lights. Ask what helps to relieve the headache. Is the patient under stress? Has he had trouble sleeping?

    Take a drug and alcohol history, and ask about head trauma within the last 4 weeks. Has the patient recently experienced nausea, vomiting, photophobia, or visual changes? Does he feel drowsy, confused, or dizzy? Has he recently developed seizures, or does he have a history of seizures?

    Begin the physical examination by evaluating the patient’s level of consciousness (LOC). Then check his vital signs. Be alert for signs of increased ICP—widened pulse pressure, bradycardia, altered respiratory pattern, and increased blood pressure. Check pupil size and response to light, and note any neck stiffness. (See Differential diagnosis: Headache, pages 392 and 393.)

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Syncope: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur?

    Next, take the patient’s vital signs and examine him for any injuries that may have occurred during his fall.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Headache: History
    (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

    A. Characteristics of the headache. What is the type of pain, its location, its duration, and its intensity? What symptoms precede or accompany the pain? Does anything trigger the headache or make the pain better or worse? Tell about a typical headache from beginning to end.

     1. Migraine food triggers include alcohol, aged cheese, chocolate, and aspartame.

     2. Approximately 20% to 30% of migraineurs will report an aura, typically visual in nature.

    3. Patients with cluster headache report unilateral temporal headache, occurring generally once daily, usually in the evening and associated with ipsilateral nasal stuffiness and conjunctival injection.

    4. Chronic daily headache (CDH) patients will describe headaches at least 10 to 15 days/month and usually report heavy use of relief drugs.

     5. Red flags that might suggest intracranial pathology (section I.B) include a loss of consciousness, persistent visual loss, seizures, staggering, or hearing loss.

     B. Chronology of the headache. Most primary headaches recur periodically for years, with only subtle changes over time. If the headache is getting worse, the cause might be psychosocial stressors, medication overuse, or evolving intracranial pathology (Table 2.5). Ask women whether the headache seems related to the menses. Past and current medication use and how they affect the headache can be important clues to headache severity and how the patient may respond to treatment.

     C. Family history. Migraine headaches often exhibit a familial pattern; the causes of secondary headaches generally do not. Tension headache can represent a family pattern of reacting to stress.

    D. Psychosocial aspects of the headache. What does the patient believe is the cause of the headache? What life events might be playing a role? How does the patient’s family react to the headache? Ask: “If you did not have the headache, how would your life be different?” The key to management of recurrent primary headaches often lies in the responses to these questions, which can reveal unanticipated stressors, secondary gain, or family discord.

    E. Other information. Important data include use of tobacco, alcohol, or coffee; response to exercise; a history of head trauma; or exposure to toxic fumes or chemicals. Have there been symptoms of fever, or fatigue? Ask about depression, which is often seen in migraineurs.

    Physical examination

     A. Focused physical examination (PE). This should include vital signs (notably blood pressure) and an examination of the scalp; eyes, including funduscopic examination; ears; nose; paranasal sinuses; throat; and neck. A screening neurologic examination, including cranial nerves, coordination (finger-to-nose test), and deep tendon reflexes, is sufficient in most instances. In the migraineur, the examination findings should be all normal in the absence of a current headache; a positive finding warrants further testing (section IV).

    B. Additional PE. Other PE maneuvers are appropriate if the medical history suggests specific secondary headache causes: palpation of the superficial temporal arteries (temporal arteritis), audiometry (acoustic neuroma), transillumination of the paranasal sinuses (“sinus headache”), or checking for nuchal rigidity plus Kernig’s and Brudzinski’s signs (meningeal irritation).

    » READ BOOK EXCERPT ONLINE »

    Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

    Syncope: History
    (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

    A. What are the symptoms or circumstances related to the syncope?

    1. Dizziness preceding syncope is highly associated with a psychological cause (24%) versus syncope without preceding dizziness (5%) (3). Dizziness with syncope can also be associated with arrhythmia.

    2. Important history includes palpitation, duration of prodrome and recovery, and presence of postural or exertional symptoms.

    3. Related environmental factors include heat, dehydration, and alcohol.

    B. Which disease, risk factor, or family history is present?

    1. Organic heart disease is associated with arrhythmia and increased risk of death.

     2. Psychiatric illnesses most commonly associated with syncope are major depression (12.2%), alcoholism (9.2%), generalized anxiety disorder (8.6%), and panic disorder (4.3%). These correlate with a higher rate of recurrent syncope, younger age, and a more benign course (4) (Chapters 3.1 and 3.3).

     3. Older age (>60 years) is more highly associated with arrhythmias, orthostatic hypotension, medication side-effects, and situational (e.g., micturition) syncope.

     4. Ask about diabetes mellitus, neuropathy, anemia, and other chronic diseases.

     5. Inquire about a family history of sudden death, hypertrophic cardiomyopathy, or other organic heart disease.

    C. What medicines does the patient take? The most commonly implicated are antihypertensives and antidepressants. Others include antianginals, analgesics, and sedatives.

    Physical examination

    What are the essential aspects to cover?

    A. General: mental status, temperature, hydration status, pallor, or cyanosis.

     B. Vital signs: tachycardia, bradycardia, irregularity, or orthostatic hypotension.

     C. Cardiovascular: heart sounds, murmurs, bruits, edema, rales, and pulses.

     D. Neurologic: cranial nerves, reflexes, strength and sensation, tremor, Romberg’s sign, gait, and cerebellar signs.

    » READ BOOK EXCERPT ONLINE »

    Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

    Headache: Differential Overview
    (Field Guide to Bedside Diagnosis)

    ❑ Migraine

    ❑ Tension

    ❑ Acute sinusitis

    ❑ Acute glaucoma

    ❑ Postconcussive

    ❑ Cluster

    ❑ Meningitis

    ❑ Drugs

    ❑ Hypoglycemia

    ❑ Benign exertional headache

    ❑ Temporomandibular joint inflammation

    ❑ Subdural hematoma

    ❑ Subarachnoid hemorrhage

    ❑ Acute epidural hematoma

    ❑ Lumbar puncture

    ❑ Brain tumor

    ❑ Headache in HIV

    ❑ Pseudotumor cerebri

    ❑ Hypertensive encephalopathy

    ❑ Carbon monoxide intoxication

    ❑ Giant cell arteritis

    ❑ Psychogenic

    ❑ Brain abscess

    ❑ Encephalitis

    ❑ Arteriovenous malformations

    ❑ Cavernous sinus thrombosis

    ❑ Pituitary apoplexy

    ❑ Carotid artery dissection

    Diagnostic Approach

    Red flags to serious causes include: Sudden onset of “the worst headache of my life,” especially in a non—headache-prone person; headache different from previous headaches; headache precipitated by position change, cough, or exertion; a history of trauma or fever; abnormal mental status or other neurological findings; a headache that disturbs sleep or is present immediately on awakening; immune deficiency such as HIV.

    The time course helps in diagnosing headache. A “thunderclap” headache of a ruptured aneurysm peaks instantly. Cluster headache peaks over 3 to
    5 minutes, remains at maximum for 45 minutes, and then gradually recedes. Migraine builds over hours, lasts hours to days, and is improved with sleep.

    In evaluating patients with recurrent migraine, it is critical to ascertain whether the present headache differs from prior migraines and whether fever is present or spontaneous retinal venous pulsations are abnormally absent. These should prompt a search for alternative causes. If fever is present with headache, rule out meningitis.

    Raised intracranial pressure should be suspected with blurred vision upon bending the head forward, headache upon awakening that improves with sitting up, double vision, loss of coordination and balance, or daily
    progressive headache with nausea. Pain originating above the tentorium is referred to the frontal, temporal, or parietal region. Pain from the posterior fossa and below is referred to the occiput. Pain from the posterior sagittal and transverse sinuses may be referred to the eye or forehead.

    Lumbar puncture, subdural hematoma, or benign intracranial hypertension can cause orthostatic headache. Occipital headache radiating to the vertex and forehead is usually a result of cervical spondylosis but can also be caused by basal subarachnoid hemorrhage, posterior fossa tumor, or meningitis.

    » READ BOOK EXCERPT ONLINE »

    Source: Field Guide to Bedside Diagnosis, 2007

    Syncope: Differential Overview
    (Field Guide to Bedside Diagnosis)

    Orthostatic/Autonomic

    ❑ Neurally mediated hypotension

    ❑ Volume depletion

    ❑ Cough syncope

    ❑ Anemia

    ❑ Autonomic insufficiency

    Cardiac/Obstructive

    ❑ Myocardial infarction

    ❑ Pulmonary embolism

    ❑ Aortic stenosis

    ❑ Hypertrophic obstructive cardiomyopathy

    ❑ Aortic dissection

    ❑ Cardiac tamponade

    ❑ Left atrial myxoma

    Cardiac/Dysrhythmic

    ❑ Complete heart block

    ❑ Sick sinus syndrome

    ❑ Tachyarrhythmia

    ❑ Carotid sinus hypersensitivity

    Neurologic

    ❑ Vertebrobasilar ischemia

    ❑ Hypoglycemia

    ❑ Unwitnessed seizure

    ❑ Subclavian steal syndrome

    Psychologic

    ❑ Hyperventilation

    ❑ Hysterical faint

    Diagnostic Approach

    The cause of syncope is usually evident after a careful history and physical exam. Identification of a cardiac cause is critical because it portends a poor prognosis (1-year mortality 18% to 33%). In patients with heart disease, the most specific predictors of a cardiac cause are syncope in the supine position or during effort, blurred vision, and convulsive syncope. In patients without heart disease, palpitations are the only significant predictor of a cardiac cause.

    Focus on preceding events and witness description. Sudden loss of consciousness without warning is usually due to an arrhythmia. Syncope with chest pain mandates that aortic dissection, myocardial infarction, and pulmonary embolism be ruled out. Syncope with exertion suggests aortic stenosis, hypertrophic obstructive cardiomyopathy, or bradycardia. Events after the syncope, such as confusion, lethargy, or neurological symptoms suggest a seizure.

    Consider syncope as the cause of unexplained trauma such as hip fracture or MVA.

    » READ BOOK EXCERPT ONLINE »

    Source: Field Guide to Bedside Diagnosis, 2007

    Headache: Diagnosis
    (Handbook of Diseases)

    An accurate diagnosis requires a history of recurrent headaches and physical examination of the head and neck. Such examination includes percussion, auscultation for bruits, inspection for signs of infection, and palpation for defects, crepitus, and tender spots (especially after trauma).

    A firm diagnosis also requires a complete neurologic examination, assessment for other systemic diseases (such as hypertension), and a psychosocial evaluation (when such factors are suspected).

    Most patients may be diagnosed by a thorough history and physical examination. Magnetic resonance imaging, computed tomography scans, lumbar puncture, and serology may be beneficial. Neurologic deficits, such as stroke or brain tumors; metabolic processes, such as thyroid disease or diabetes; and an aneurysm must be ruled out if the headache is explosive and “the worst” in their lives.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Diseases, 2003

    Premenstrual syndrome: Diagnosis
    (Handbook of Diseases)

    The patient history shows typical symptoms related to the menstrual cycle. To help ensure an accurate history, the patient may be asked to record menstrual symptoms and body temperature on a calendar for 2 to 3 months before diagnosis.

    Estrogen and progesterone blood levels aren’t clinically useful. A psychological evaluation is recommended to rule out or detect an underlying psychiatric disorder.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Diseases, 2003

    Syncope: History
    (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

    Ask the patient for information about the fainting episode. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he stand quickly from a sitting or prone position? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur?

    Physical examination

    Perform a complete cardiac and neurologic examination. Provide continuous cardiac monitoring. Next, take the patient’s vital signs and examine him for injuries that may have occurred during his fall.

    » READ BOOK EXCERPT ONLINE »

    Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

    Aura: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    Obtain a thorough history of the patient’s headaches or seizure history, asking him to describe any sensory or motor phenomena that precede each headache or seizure. Find out how long each headache or seizure typically lasts. Does anything make it worse, such as bright lights, noise, or caffeine? Does anything make it better? Ask the patient about drugs he takes for pain relief.

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Headache: History

    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    If the patient reports a headache, ask him to describe its characteristics and location. How often does he get a headache? How long does a typical headache last? Try to identify precipitating factors, such as certain foods or exposure to bright lights. Ask what helps to relieve the headache. Is the patient under stress? Has he had trouble sleeping?

    Take a drug and alcohol history, and ask about head trauma within the last 4 weeks. Has the patient recently experienced nausea, vomiting, photophobia, or visual changes? Does he feel drowsy, confused, or dizzy? Has he recently developed seizures, or does he have a history of seizures?

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Syncope: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur?

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Headache: Clinical Features and Diagnosis
    (The Diagnostic Approach to Symptoms and Signs in Pediatrics)

    Tension-Type Headache

  • Most commontype of headache in adolescence but also occurs in childhood.
  • Usually dull in character, diffuse,and bilateral and may last hours or days.
  • Nausea and vomiting are unusual.
  • Precipitating factors include emotionalstress and fatigue.

    • Vascular Headache

    Migraine Headache

  • Vascularheadaches that are periodic, throbbing, and usually unilateral.
  • Generalized headaches are more commonthan unilateral headaches in children.
  • Positive family history is found inmany cases.
  • Typical clinical features and positivefamily history are diagnostic.

    • Migraine with Aura (Classic Migraine)

  • Migraineheadaches that occur with aura are called classic migraine.
  • Not only does aura precede headache,but it can persist with headache. May consist of visual (scotomata,flashing lights, blurring), sensory (numbness, paresthesias), ormotor (mild aphasia) phenomena.
  • Headache usually lasts for a few hoursbut can persist for 1–2 days. Interrupts normal activity,and most children wish to lie down in quiet place until it goesaway. Noise, light, and activity make headache worse.

    • Migraine without Aura (Common Migraine)

  • Migraineheadaches that occur without aura are called common migraines.
  • In childhood they are more common thanclassic migraines.
  • Headache is bifrontal or bitemporaland is often associated with nausea, vomiting, and abdominal pain.
  • Positive family history for migraineis important diagnostic clue.

    • Complicated Migraine

  • Associationof migraine episode with transient neurologic disturbance.
  • Deficits are usually benign but mustbe distinguished from serious intracranial pathology; thus, headCT or MRI is often necessary.

    • Hemiplegic Migraine

  • Hemisensoryloss or hemiparesis followed by headache on contralateral side characterizeshemiplegic migraine, which can be familial.
  • Hemiplegia may persist after headacheresolves and lasts hours to days. Can recur and alternate from sideto side. Permanent deficit rarely occurs.

    • Ophthalmoplegic Migraine

  • Associationof recurrent, unilateral, periorbital headaches associated withthird nerve palsy is known as ophthalmoplegic migraine.
  • Headache may precede, accompany, orfollow ophthalmoplegia. Eyes appear "down and out," withdeficits in elevation and adduction. There also may be ptosis andmydriasis.
  • Headache may last a few hours, butophthalmoplegia can persist for days to weeks.

    • Basilar Artery Migraine

  • Often beginswith visual disturbance consisting of blurred vision, scotomata,or transient loss of vision. Nausea, vomiting, ataxia, vertigo,paresthesias, hemiparesis, quadraparesis, and impaired consciousnessalso can occur.
  • Occipital headache may precede, accompany,or follow neurologic deficits. Episode lasts usually 10–30mins.
  • Recurrent attacks with absence of residualneurologic deficits is general pattern.

    • Confusional Migraine

  • Headacheusually precedes episodes of confusion that last a few hours upto 1 day. Impaired memory and restless or combative behavior sometimesoccur.
  • There is often family history of migraineheadache.
  • Diagnosis is usually made retrospectively.

    • Migraine Variants

  • Migrainevariants refer to transient episodic neurologic dysfunction in individuals withmigraine or who later develop migraine.
  • Cyclic vomiting is episodic occurrenceof unexplained nausea, vomiting, and abdominal pain that may occur ± headache.
  • Paroxysmal torticollis consists ofrecurrent episodes of torticollis, which are associated with nausea,vomiting, and headache that may last from hours to days.
  • Benign paroxysmal vertigo is suddenonset of vertigo, lasting a few minutes, and usually occurring inchildren 2–6 yrs of age. Children are frightened and unableto stand but do not lose consciousness.

    • Cluster Headache

  • Form ofvascular headache that may be transmitted as autosomal-dominanttrait in some cases.
  • Onset is usually in children >10yrs of age.
  • Headaches are intense, unilateral,and periorbital in location. Occur 2–10 times/day,lasting from 10 mins to a few hours, and never switch sides.
  • Headaches are usually episodic, occurringfor 1–3 mos at a time with remissions that last monthsto years.

    • Systemic Infection

    Any systemic infection, usually viral orbacterial, may produce fever and headache.

    Hypoxia

    Can cause vasodilatation of cerebral arteriesand produce headache. Frequent causes include high altitude, carbonmonoxide poisoning, and chronic lung disease (most commonly cysticfibrosis).

    Systemic Hypertension

    When severe, may cause headache, which canbe dull or throbbing. BP should be measured in anyone who complainsof persistent severe headache.

    Connective Tissue Diseases

    Systemic lupus erythematosus may cause cerebralvasculitis and headache.

    Head Trauma

  • Minor headtrauma can produce bruising, soft-tissue swelling, and mild headache. Whiplashinjuries produce neck pain, stiffness, and often occipital headache.
  • Concussion-associated headache generallylasts for a few days.
  • Postconcussion syndrome is unusualin childhood but may last for months or years. Besides headache,dizziness, irritability, insomnia, memory loss, and learning difficultiesalso may occur.

    • Headache Due to Disorders of Head and Neck Structures

    Headache often occurs with various disordersinvolving head and neck region. History, physical exam, and appropriateradiographs are usually diagnostic.

    Head and Neck Disorders

  • Other causesof cranial headache include osteomyelitis of skull and cervicalspine disorders (congenital anomalies, fracture, bone tumor, juvenilerheumatoid arthritis).
  • See section Head Trauma.

    • Ear, Eye, and Sinus Disorders

  • Acute otitismedia can produce headache, but earache and fever are major manifestations.
  • Hyperopia and astigmatism are occasionallyassociated with sustained contraction of extraocular, frontal, andtemporal muscles, which can cause frontal headache.
  • Acute glaucoma is characterized byincrease in intraocular pressure and steady pain in eye region,which may radiate to forehead.
  • Eye strain is another cause of ocularpain and headache.
  • In young children, headache from sinusdisease is uncommon. In older children, acute and chronic sinusitiscan cause frontal headache along with tenderness over involved sinus.Maxillary and ethmoid sinuses are most commonly involved. Pain isusually dull, aching, and nonthrobbing.

    • Mouth and Jaw Disorders

    Dental caries, malocclusion, and temporomandibularjoint dysfunction sometimes cause pain in frontal and temporal areasas well as jaw pain.

    Intracranial Infections

  • Headachewith meningitis or encephalitis is usually acute, constant, generalized,and associated with fever.
  • Brain abscess may produce headacheif abscess is large enough to cause traction and displacement ofintracranial structures. Associated findings include fever, vomiting,seizures, papilledema, hemiparesis, and alteration in consciousness.CT and MRI are usually diagnostic.
  • See Chap.3, Alteration in Consciousness.

    • Traction Headache

    Pain-sensitive intracranial structures includecerebral and dural arteries and large cerebral veins and venoussinuses. Traction on these structures produces headache.

    Brain Tumor

  • Headachesin children with brain tumors may be throbbing or nonthrobbing.
  • Although pain-free intervals sometimesoccur, these headaches are usually persistent and become more intense.
  • Also common for these headaches toawaken children from sleep and to occur upon awakening in morning.
  • Vomiting, lassitude, visual disturbance,ataxia, seizures, personality change, neck stiffness, papilledema,and alteration in consciousness can be manifestations of brain tumor.
  • Response to analgesics is unreliableindicator for presence of tumor.
  • CT or MRI locate and define extentof tumor. Histologic diagnosis is definitive.
  • Table25.1 lists common brain tumors and their locations.

    • » READ BOOK EXCERPT ONLINE »

    Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

    Syncope and Dizziness: Clinical Features and Diagnosis
    (The Diagnostic Approach to Symptoms and Signs in Pediatrics)

    Cardiovascular Syncope

    Neurocardiogenic Syncope (Common Faint)

  • Most commontype of syncope in childhood and adolescence.
  • Often a response to anxiety, fear,pain, or other emotional stress.
  • Also may occur after extreme fatigue,prolonged standing, or fasting.
  • Pathogenesis involves vasodilatationof skeletal muscle vasculature and failure of heart rate and strokevolume to maintain cardiac output for adequate cerebral blood flow.
  • Dizziness, nausea, sweating, and abdominaldiscomfort may precede syncope. Interruption of cerebral perfusionfor 2–3 secs produces dizziness, but lying down duringpresyncopal phase may prevent syncopal episode.
  • If cerebral perfusion is interruptedfor >10 secs, syncope occurs.
  • Onset is sudden with hypotension (vasodepressorresponse), and BP decreases to ≤60 mm Hg. Bradycardia usuallyoccurs, and often junctional rhythm or period of asystole (cardioinhibitory response)may follow.
  • Most episodes are associated with uprightposition, and child becomes limp and falls to ground. Loss of consciousnessusually lasts <1 min.
  • Seizures are unusual but may occurwith prolonged syncope.
  • Once individual is horizontal, BP,heart rate, and color return toward normal.
  • History and physical exam are usuallydiagnostic. Individuals with this form of syncope do not need furthertesting unless syncope is recurrent, when tilt table testing mayconfirm its presence.
  • Both tussive and micturition syncopeare now considered forms of neurocardiogenic syncope.

  • Tussive syncopehas been attributed to large increase in intrathoracic pressure,which decreases venous return to the heart. It may occur after significantcoughing of any cause, but especially after severe paroxysmal coughingwith pertussis.
  • Micturition syncope is most commonin elderly men, but it can occur in older adolescents. Syncope usuallyoccurs at the end of micturition. The mechanism is unclear, buta full bladder causes peripheral vasoconstriction, and with emptying,peripheral vasodilatation occurs, which in the erect posture mayproduce syncope.

    • Cardiac Syncope

    Congenital and Acquired Heart Disease

  • Syncopemay occur with outflow obstruction of left ventricle (LV) (valvar,subvalvar, or supravalvar aortic stenosis; hypertrophic cardiomyopathy),outflow obstruction of right ventricle (RV) (pulmonic stenosis,primary pulmonary artery hypertension, pulmonary vascular disease),inflow obstruction of LV (mitral stenosis, atrial myxoma), and inflowobstruction of RV (cardiac tamponade). More likely to occur duringor just after physical exertion, when cardiac output cannot increaseenough to meet demands of oxygen delivery to brain.
  • Syncope also may occur with cardiomyopathy,myocarditis, and endocarditis as a result of decreased cardiac output.
  • Another cause is myocardial ischemia,which may occur with coronary artery anomalies, especially anomalousorigin of left coronary artery from pulmonary artery and abnormalcourse of left coronary artery between aortic and pulmonary trunkswith compression of artery during exercise. Coronary artery aneurysmsand thrombosis found in Kawasaki disease also may produce myocardialischemia and syncope.
  • In most cases, history, physical exam,chest radiograph, ECG, and 2-D echocardiogram are diagnostic.
  • Diagnosis of primary pulmonary hypertensionusually requires lung biopsy to exclude pulmonary venoocclusivedisease. Although pulmonary vascular disease may be diagnosed clinicallywith support of echocardiography, cardiac catheterization and angiographycan confirm these findings.

    • Hypercyanotic Episodes

  • Consistof intense cyanosis and hyperpnea. Occur most commonly with tetralogyof Fallot but also can occur with tricuspid atresia, transpositionof great arteries with pulmonary stenosis, and pulmonary vasculardisease.
  • Children who can walk may squat duringepisode, which increases systemic vascular resistance and decreasesright-to-left shunt.
  • Occasionally episodes may be prolongedand associated with syncope and seizures. During episode, murmuris less intense or disappears.
  • Several factors seem to play a role:prolonged crying with decreased venous return, constriction of RVinfundibulum, decreased systemic vascular resistance secondary toimmobilization or spontaneous vasomotor changes, relative anemia,and increased physical activity with higher oxygen requirement.

    • Arrhythmias in Structurally Normal Heart

  • Syncopemay occur from sinus bradycardia, junctional bradycardia, second-and third-degree (atrioventricular) AV block with low ventricularrate, supraventricular tachycardia, atrial flutter, or ventriculartachycardia.
  • Atrial fibrillation with rapid ventricularresponse over the accessory pathway may be associated with syncopeor near syncope in Wolff-Parkinson-White (WPW) syndrome. Diagnosisis usually confirmed by ECG, which shows short PR interval and deltawave.
  • Syncope also may occur with prolongedQT interval, in which variable recovery time with reentry depolarizationmay cause torsade de pointes ventricular tachycardia.

  • ProlongedQT interval has a number of genetic causes. Hypokalemia, hypocalcemia, andhypomagnesemia also may cause QT interval prolongation. Tricyclicantidepressants and phenothiazines have been associated with prolongedQT interval, and so have overdoses of quinidine, procainamide, anddisopyramide.
  • Prolonged QT interval can be diagnosedby measuring this interval on routine ECG, but it must be correctedfor heart rate. 1 method for correction of QT interval is to measureQT interval (in secs) and divide by the square root of the RR interval(in secs). In 95% of individuals, the corrected QT interval is <0.45secs.
  • Sympathomimetic drugs when taken inlarge doses or from idiosyncratic reaction may produce supraventricularor ventricular tachycardia. Cocaine also may produce ventriculartachycardia and syncope. Metabolic derangements (e.g., hyperkalemia,hypoglycemia, and hypercalcemia) also may result in syncope by producingarrhythmias, but this is rare.
  • ECG may be diagnostic of these arrhythmias.If syncopal episodes are frequent, Holter monitoring may be useful;if they occur during exercise, maximal exercise testing may be diagnostic.Otherwise, event recorder or implanted loop recorder should be considered.
  • If syncope still remains unexplained,electrophysiologic studies should be performed.

    • Arrhythmias in Structurally Abnormal Heart

  • Childrenwho have congenital or acquired heart disease are at risk for arrhythmias thatmay produce syncope. These include sinus bradycardia, sick sinussyndrome, supraventricular tachycardia, atrial fibrillation, atrialflutter, ventricular tachycardia, ventricular fibrillation, andcomplete heart block.
  • WPW syndrome and supraventricular tachycardiaare occasionally associated with Ebstein anomaly.
  • Complete heart block may be associatedwith ventricular inversion and transposition of great arteries.
  • Ventricular tachycardia may occur fromarrhythmogenic RV dysplasia, although echocardiography may not bediagnostic because a heavily trabeculated RV may be indistinguishablefrom dysplasia. Recurrent ventricular tachycardia, especially exercise-induced,and left bundle branch pattern suggest this diagnosis, which canbe confirmed by MRI.
  • Children who have had surgical repairof a cardiac defect are also at risk for development of arrhythmias.An incision in the ventricle is a risk factor for ventricular tachycardia.Supraventricular tachycardia, atrial fibrillation, atrial flutter,sick sinus syndrome, and ventricular tachycardia may occur after Mustardor Senning procedure for repair of transposition of great arteries.Surgical manipulation in the area of sinus or AV nodes in repairof AV canal defects, posterior ventricular septal defects, or tunnelaortic stenosis may predispose to development of sinus bradycardiaand heart block.
  • ECG may be diagnostic of these arrhythmias.Holter monitoring and maximal exercise testing also may be helpfulin diagnosis.
  • If these tests are normal consideringhigher risk of life-threatening events in children with structurallyabnormal hearts, electrophysiologic studies should be considered.

    • Vascular Syncope

    Orthostatic Syncope

  • Occurs whenindividual assumes upright posture and systolic arterial BP decreasesby ≥15 mm Hg.
  • Possible causes include

  • Decreasedblood volume (blood loss, GI fluid loss, excessive diuretic use)
  • Failure of normal postural reflexes(suddenly standing up after prolonged bedrest, familial dysautonomia,spinal cord lesions)
  • Drugs (vasodilators, tricyclic antidepressants,sedatives, opiates, cocaine)
  • Supine and standing BPs should be measuredin any individual with unexplained syncope.

    • Cerebrovascular Syncope

  • This typeof syncope may be due to excessive vagal stimulation, which causessevere bradycardia or AV block.
  • Examples include intubation, placementof nasogastric tube or esophageal overdrive pacing catheter, removalof pleural or peritoneal fluid, and distention of viscera.
  • Excessive vagal tone also may occurin normal adolescents or well-trained athletes, and a further increasein vagal tone may worsen bradycardia or AV block enough to causesyncope.

    • Carotid Sinus Syncope

    Pressure on baroreceptors in carotid sinusmay cause carotid sinus syncope. Uncommon in children but can occurwith excessive pressure on neck (e.g., wearing tight collar).

    Noncardiovascular Syncope

    Breath-Holding

  • Common inchildren 6 mos–6 yrs of age. Precipitating factors includepain, frustration, and anger.
  • Pallid breath-holding, which is nowthought to be variation of neurocardiogenic syncope, usually followsacute pain or injury. The infant or child becomes pale and losesconsciousness. Complete recovery occurs in 1–2 mins.
  • More common is cyanotic breath-holdingspell in which infant or child cries, holds breath during expiration,and turns dusky until breathing begins again. Loss of consciousnessand tonic-clonic movements may occur with prolonged episode.

    • Hyperventilation

  • Frequentcause of dizziness but rare cause of syncope.
  • Common in adolescent girls and usuallydue to emotional stress.
  • Frequent complaints include lightheadedness,blurred vision, difficulty breathing, choking, smothering, chesttightness, and numbness or tingling of fingers, toes, and face.Individuals who are hyperventilating appear anxious and have fastand deep respirations.
  • Rebreathing into paper bag and thoughtfulreassurance usually lessen hyperventilation, so that individualscan begin talking about what is upsetting them.

    • Migraine

    Severe migraine headache may cause syncopalepisode, especially if basilar arterial system is affected (see Chap. 25, Headache).

    Metabolic

    Hypoxia Including Anemia

    Severe hypoxia or severe anemia of any causemay result in syncope. See Chap.45, Pallor (Anemia), and Chap. 56, Respiratory Distress and Apnea.

    Hypoglycemia

  • Often causesfaintness and dizziness, but syncope is exceedingly rare. Othermanifestations of hypoglycemia include headache, hunger, sweating,and jitteriness, which may progress to confusion, seizures, andcoma.
  • Low blood glucose level confirms presenceof hypoglycemia.
  • With administration of oral or intravenousglucose, symptoms resolve.
  • See further discussion of hypoglycemiain Chap. 59, Seizures.

    • Psychologic

  • Acute stressmay produce anxiety and syncope with or without hyperventilation. Commonstresses are witnessing a tragic event or hearing news of the deathof close friend or relative.
  • Hysteria is common cause of recurrentfainting in adolescents, especially in those with hysterical personalities.

  • In this typeof episode, which almost always occurs in presence of other people,hysterical person falls or slumps in dramatic way but avoids injury.Fainting also may occur while lying or sitting down. There is noprodrome or change in heart rate, BP, or skin color.
  • Diagnosis of psychologic causes ismade from history, physical exam, and clinical observation.

    • Diagnostic Approach

  • Neurocardiogenicsyncope, vascular syncope, breath-holding, hyperventilation, and psychologicdisturbances can usually be distinguished by history and physicalexam.
  • If syncopal episode occurs on assumingupright posture, BP should be measured in supine and upright positions.Postural difference in systolic pressure of >15 mm Hg confirmsdiagnosis of orthostatic syncope.
  • Individuals with recurrent syncope,family history of sudden death, or syncope occurring during intensiveexercise need further evaluation.

  • If recurrent syncope occurs, tilt testingmay determine whether syncope is neurocardiogenic.
  • Family history of syncope and suddendeath suggests hypertrophic cardiomyopathy or long QT interval syndrome.
  • Syncope during intense exercise mayoccur with hypertrophic cardiomyopathy, severe aortic stenosis,anomalous left coronary artery from pulmonary artery, primary pulmonaryhypertension, or exercise-induced atrial fibrillation associatedwith WPW syndrome.
  • Diagnosis of cardiac disorders canbe made from history, physical exam, chest radiograph, ECG, and2-D echocardiogram. Cardiac catheterization and angiography maybe necessary to make definitive diagnosis and to determine severityof lesion. Arrhythmia may be suspected from history, and routine ECGwith rhythm strip may be diagnostic. Otherwise, further testingmay be needed (e.g., Holter monitoring, maximal exercise testing,event recorder or implanted loop recorder monitoring, and electrophysiologictesting).
  • With syncopal episode of unknown cause,ECG should be initially performed searching for WPW syndrome, longQT interval syndrome, or LV hypertrophy with T-wave changes indicativeof cardiomyopathy.
    • >>

    » READ BOOK EXCERPT ONLINE »

    Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

    Aura: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    Obtain a thorough history of the patient's headache or seizure history, asking him to describe any sensory or motor phenomena that precede each headache or seizure. Find out how long each headache or seizure typically lasts. Does anything make it worse, such as bright lights, noise, or caffeine? Does anything make it better? Ask the patient about drugs he takes for pain relief.

    Then perform a complete neurologic examination.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Headache: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    If the patient reports a headache, ask him to describe its characteristics and location. How often does he get a headache? How long does a typical headache last? Does he have a history of high blood pressure? Try to identify precipitating factors, such as certain foods or exposure to bright lights. Ask what helps to relieve the headache. Does he experience stress at work or at home? Has he had trouble sleeping?

    Take a drug and alcohol history, and ask about head trauma within the past 4 weeks. Has the patient recently experienced nausea, vomiting, photophobia, or vision changes? Does he feel drowsy, confused, or dizzy? Has he recently developed seizures or does he have a history of seizures?

    Begin the physical examination by evaluating the patient's level of consciousness (LOC). Then check his vital signs. Be alert for signs of increased ICP—a widened pulse pressure, bradycardia, an altered respiratory pattern, and increased blood pressure. Check pupil size and response to light, and note any neck stiffness.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Syncope: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur? Obtain a complete drug history.

    Next, take the patient's vital signs and examine him for any injuries that may have occurred during his fall. Place him on a cardiac monitor and assess his heart rhythm for abnormalities. Assess cardiac and respiratory status. Monitor pulse oximetry. Perform a neurologic examination.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    SYNCOPE: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    Clinical differentiation of the various forms of syncope is made by combinations of symptoms. Thus, syncope with marked sweating and tachycardia is more likely due to hypoglycemia. Syncope with sweating and bradycardia is more likely due to vasovagal syncope. Focal neurologic signs during the attack suggest transient ischemia attack (TIA) and prompt a search for sources of emboli or thrombosis (sickle cell disease, polycythemia, or macroglobulinemia). Transesophageal echocardiography is the procedure of choice to find a cardiac source. A family history of syncope suggests migraine, epilepsy, or vasovagal attacks. Epilepsy is a strong possibility in the young, whereas heart block is more likely in the aged. Consequently, an EEG and Holter monitoring are useful in the workup.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007


     » Next page: Signs of Basilar artery migraine

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