Ophthalmologic Manifestations of Pediatric Headache Clinical Presentation

  • Author: Marc E Lenaerts, MD, FAHS; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Jan 27, 2010
 

History

Besides the impairment caused by the headache itself, pediatric patients are seen by a physician because of parental concerns.

In 25% of patients, the physician is a pediatric neurologist, but frequently another specialist may be the initial consultant, because symptoms may suggest an underlying cause. Often, it will be the ophthalmologist who is the initial consult, because migraine presents with prominent or worrisome visual symptoms.

It is crucial to address the child with age-appropriate language. For the very young, the use of visual materials and asking the child to draw the headache or other symptoms can be very helpful.

  • No formal classification exists for headaches specific to children. Improving on the initial classification of 1988, although still far from ideal, is a new classification of headache disorders that was published in 2004 by the International Headache Society, as part of the second edition of the International Classification of Headache Disorders (ICHD-II).[16, 17, 18, 19]
    • However, many unique aspects of childhood syndromes are not mentioned and have been emphasized in epidemiologic studies, such as that of Wober-Bigol et al. In particular, lack of throbbing, absence of lateralization, and shorter duration of the attack are common differences when compared with adult presentation of migraine.[20]
    • A proposed revision includes changing the minimum duration from 4 hours to 1 hour and changing the character "unilateral" into "either bilateral or unilateral." Chakravarty et al showed that the onset of headache in pediatric patients is commonly holocranial, as opposed to the unilateral or vertex onset in adults. Only about 1 in 10 children with headache complains that the pain is unilateral. Winner et al proposed a revised version in 1995. If wider time criteria for migraine attacks are adopted, as in DeGrauw et al, a significant increase will occur in the incidence of migraine.[21, 22, 23]
  • One of the most important features to inquire about is the notion of recurrent and fairly stereotyped episodes of head pain associated with autonomic dysfunction. The latter are frequently at the forefront of the clinical picture with little or no headache. Autonomic dysfunction consists of nausea, vomiting, dizziness, hypotension, bradycardia, pallor, diaphoresis, and diarrhea. Syncope can even be part of the picture, to distinguish from the loss of consciousness as part of the aura in basilar migraine.
  • The essential symptomatology of migraine is the attack, which consists of the following features:
    • Prodromes or premonitory symptoms typically occur between one or more hours (rarely a few days), before onset of the pain phase. Most symptoms point to a hypothalamic dysfunction. Premonitory symptoms include mood changes (depression, irritability, rarely elation), changes in appetite (hunger and especially craving for sweets), alteration in arousal (tiredness, yawning), or altered water balance (polydipsia, thirst).
    • Aura only occurs in migraine with aura, which represents about a fifth of all migraines. This is a sudden and self-limited neurologic dysfunction lasting generally a few minutes; sometimes several can occur simultaneously or sequentially. The following symptoms can occur:
      • Visual - Scotomas, phosphenes that look like stars, straight or broken lines (fortification spectra), colors, illusions of shape (micropsias, macropsias, dysmorphopsia), rarely hallucinations (more complex pictures)
      • Sensory - Paresthesias, rarely dysmorphopsia (impression one's body is deformed)
      • Motor - Paresis or hemiplegia, especially prominent in familial hemiplegic migraine
      • Speech or language disturbance - Dysarthria, aphasia
      • Other cognitive - Confusion or amnesia
      • All these symptoms have been attributed to cortical dysfunction. In a few instances, the aura supposedly has a brainstem origin, although it has never been proven (eg, loss of consciousness, ophthalmoparesis, vertigo).
    • Headache phase is the most obvious and well-known part of the attack and the most disabling. Often, it is the only phase the patient is aware of. The therapeutic approach mainly addresses this phase.
      • Patient often has severe pain, usually throbbing; typically covering a large area of the skull but predominates on one side.
      • Pain is worsened by physical activities such as running, bending over, or straining in the bathroom.
      • Patient complains of sensitivity to light, sound, and smells (ie, photophobia, phonophobia, and osmophobia).
      • Variable degrees of GI derangement are present such as anorexia, nausea, and vomiting.
      • An overall feeling of exhaustion exists, and the patient typically tends to rest in the recumbency position.
    • Postdromes - After the main headache phase, patients can experience fatigue, depression, and fluid loss (diuresis). This typically lasts a few hours.
  • Other variants of migraine that typically occur in children include the following:
    • Basilar-type migraine originally was described by Bickerstaff whose name sometimes is given to the syndrome. Basilar migraine typically starts in the early teens.
      • Basilar-type migraine presents with prominent aura symptoms, such as vertigo, tinnitus, diplopia, bilateral visual field defects, dysarthria, and loss of consciousness, which secondarily can be followed by a seizure. These symptoms supposedly are due to brainstem dysfunction, although it has never been proven. If hemiplegia is present, the diagnosis must be hemiplegic migraine.
      • The initial term of basilar artery migraine coined by Bickerstaff belies the fact that the role of a vascular component has never been established clearly. These patients respond better to calcium channel blockers, especially verapamil, than other drugs.
    • Familial hemiplegic migraine (FHM) often starts in childhood but continues into adulthood and is characterized by prominent motor deficits with the aura, as well as often alteration of consciousness or encephalopathy. Other neurologic deficits also are frequent.
    • Ophthalmoplegic migraine is a rare syndrome, probably fewer than 1% of migraines with aura; it involves a third nerve palsy, which curiously often takes place at the time of the resolution of the headache phase.
    • Confusional migraine has the striking and worrisome presentation of a confused and often obtunded child and can be associated with paroxysmal activities on EEG. The confusion can last for more than a day. This is of course a diagnosis of exclusion that can be based upon repeated observations and negative workup results. The boundaries between this entity and familial hemiplegic migraine are not always clear.
    • Prolonged aura and complicated migraine are terms reserved for when the aura persists, at least to some degree, beyond an hour or forever, respectively.
  • It has long been known that before they develop a clear migraine history, patients often experience manifestations in childhood that might actually already be the expression of their migraine or that of a common underlying dysfunction. These are called childhood periodic syndromes or migraine equivalents. Considerable overlapping exists between these syndromes, and several have features in common with the aura or accompanying features of migraine in its common adult forms. For example, vertigo has been observed in as many as 23% of children with clearly established migraine attacks. Migraine equivalents include the following:
    • Cyclic vomiting is characterized by repeated episodes of a few hours to a few days of vomiting, pallor and diaphoresis, photophobia, and sometimes low-grade fever, without any other explanation. It usually occurs at age 3 or 4 years. A recent appraisal shows that up to one half of patients with this syndrome have migraine diathesis.
    • Periodic colic pain episodes consist of episodic abdominal cramps with nausea, vomiting, pallor, and sometimes a specific headache. In one series, as many as 20% of migraineurs had this manifestation versus 4% of control subjects. It can be linked to lactose intolerance, which happens to be known as a potential migraine trigger.
    • Benign paroxysmal vertigo of childhood syndrome occurs in children aged 1-4 years and is expressed by brief (1-5 min) episodes of vertigo with nausea, pallor, and sweating, usually 3-4 times a month, and is self-limited. Electronystagmography is normal. Long-term follow-up study questions the true relation with migraine.
    • Benign paroxysmal torticollis is less frequent; it typically is seen in infants.
    • Motion sickness is a frequent precursor of migraine; it tends to persist through adulthood.
    • Besides the above, in some instances, febrile seizures have been suspected to be linked to that group of syndromes, although obviously significant heterogeneity is present. The prevalence of sleep disorders is increased in migrainous children and adolescents.
  • Proper assessment, besides adequate characterization of the attacks, includes an objective determination of the disability imparted by the headache. A pediatric adjustment of the migraine disability assessment score (MIDAS), called PedsMIDAS, is an excellent and easy-to-use tool and is recommended by Hershey et al.[14] Quality of life is seriously affected by headaches, especially chronic, in children and adolescents, from most standpoints: physical, psychological, and social and role function, as observed by Osterhaus et al and Powers et al.[24, 25]
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Physical

Thorough general and neurologic physical examination is necessary and particular attention should be given to signs of intracranial hypertension and mass effect.

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Causes

Etiologies of headaches can be multiple and virtually all systemic medical conditions can be accompanied by headache.

  • Distinguishing between causes and triggers is important, the latter act merely as precipitants of the headache condition, most often migraine.
  • Likewise, it should be clarified that although true migraine is a primary headache disorder, sometimes a migrainelike headache can be secondary to a metabolic or vascular disease. For instance, this is the case of MELAS (mitochondrial encephalomyopathy, lactic acidosis, stroke), a mitochondrial cytopathy, or CADASIL (cerebral autosomal dominant angiopathy with subcortical infarcts and leukoencephalopathy), a genetically determined disease of small vessels in the brain. The headache attacks in these disorders are indistinguishable from those of primary, true migraine, but, of course, the other symptoms and disease features make the difference.
  • A note should be mentioned on posttraumatic headaches because of their frequency. The acute phase usually is not a significant concern because it does not change the initial assessment or management; this headache phase usually is considered nociceptive. However, later, it can become a chronic, lingering head pain. This syndrome is variably associated with autonomic symptoms and often akin to a primary headache syndrome, such as migraine and tension-type headache. It is believed that the trauma has acted as a trigger or exacerbating factor in the genesis of that primary headache. Frequently, psychologic disturbances are present and need to be specifically addressed for therapeutic success.
  • Ear, nose, and throat (ENT) causes should be considered, although it likely will not be high on the list.
  • Toxic causes have to be reviewed as well, including medications.
  • Other diagnostic considerations
    • Often suspected, rarely implied, sinusitis has to be ruled out, although typically acute sinusitis presents with systemic and otorhinolaryngology (ORL) symptoms and signs and chronic or allergic sinusitis almost never are responsible for headaches.
    • Tumors, especially in the posterior fossa, are to be kept in mind, although neurologic abnormalities will be at the forefront of the clinical picture. Although rarely involved, refractive abnormalities potentially can be considered.
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Contributor Information and Disclosures
Author

Marc E Lenaerts, MD, FAHS  Staff Neurologist, Mercy Medical Group, Sacramento, CA; Associate Clinical Professor of Neurology, Department of Neurology, University of California at Davis, Sacramento

Marc E Lenaerts, MD, FAHS is a member of the following medical societies: American Academy of Neurology, American Headache Society, and International Headache Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael J Bartiss, OD, MD  Medical Director, Ophthalmology, Family Eye Care of the Carolinas

Michael J Bartiss, OD, MD is a member of the following medical societies: American Academy of Ophthalmology, American Academy of Pediatrics, American Association for Pediatric Ophthalmology and Strabismus, and North Carolina Medical Society

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD  Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Brian R Younge, MD  Professor of Ophthalmology, Mayo Clinic School of Medicine

Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

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  90. [Best Evidence] Winner P, Pearlman EM, Linder SL et al. Topiramate for migraine prevention in children: a randomized, double-blind, placebo-controlled trial. Headache. 2005;45:1304-12. [Medline].

  91. Winner P, Rothner AD, Saper J, Nett R, Asgharnejad M, Laurenza A, et al. A randomized, double-blind, placebo-controlled study of sumatriptan nasal spray in the treatment of acute migraine in adolescents. Pediatrics. Nov 2000;106(5):989-97. [Medline].

  92. [Best Evidence] Winner P, Rothner AD, Wooten JD, Webster C, Ames M. Sumatriptan nasal spray in adolescent migraineurs: a randomized, double-blind, placebo-controlled, acute study. Headache. Feb 2006;46(2):212-22. [Medline].

  93. Yarnitsky D, Goor-Aryeh I, Bajwa ZH. 2003 Wolff Award: Possible parasympathetic contributions to peripheral and central sensitization during migraine. Headache. Jul-Aug 2003;43(7):704-14. [Medline].

 
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Trigeminovascular system.The trigeminal nerve fibers around basal cerebral and meningeal vessels are triggered (various stimuli are possible), and a vicious circle starts where the nerve terminals release calcitonin gene-related peptide (CGRP), substance P, vasoinhibitory peptide (VIP), and other mediators of local neurogenic inflammation and vasodilatation. The latter further stimulates the nerve endings. On the other end of the nerve, painful messages are transmitted toward central centers, including thalamus and cortex, and the sensation of pain arises.Modern drugs, such as the triptans, act at 3 levels, via 5-HT 1 B and D receptors; they vasoconstrict the vessels, they reduce the release of the above-mentioned mediators, and they decrease the central transmission of pain impulses.
 
 
 
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