When a new headache occurs, particularly in an adult who has never been prone to headache and in which atypical features are present, such as persistent focal pain, then disorders other than migraine should be carefully ruled out. When obvious disease of cranial or extra cranial structures accompanies the headache, little diagnostic confusion results. However, when cephalgia persists without readily apparent reason, further evaluation is needed.

General physical and neurologic examination in patients with migraine, aside from the complicated varieties, is normal.  Conditions which may be confused with each of the migraine syndromes described previously will be briefly reviewed. 

Migraine without aura, as emphasized earlier, should not be diagnosed simply by the presence of headache.  Tension or muscle contraction headache alone or in combination with a vascular component is most often confused with common migraine.  The periodicity, associated symptoms (nausea, photophobia, and fluid retention), and family history all weigh in favor of migraine.  Persistent pain, absent family history, muscle tenderness, and bizarre descriptions such as "a knife being driven through the skull" raise the possibility of muscle contraction or psychogenic headache.  Any neurologic abnormality on examination, such as mild hemiparesis, consistent sensory defect, or reflex asymmetry, again suggests the possibility of intracranial disease and traction headache. Headache from intracranial sources is produced most often by inflammation, traction and displacement, or distension of pain‑sensitive structures, usually dura and blood vessels. Exact correlation of headache site with intracranial mass lesions is often misleading; but in general, lesions of the posterior fossa produce occipital headache, and hemispheric tumors produce more anterior, frontal headache.  In the absence of increased intracranial pressure, the headache tends to be localized to the side of the lesion. 

Cranial arteritis, a disorder of the elderly, often produces headache, frequently without overt signs.  The headache can be severe and accompanied by tenderness of the extra cranial arteries.  In the older patient the investigation of a new headache should always include a sedimentation rate as a screening test for cranial arteritis.

Migraine with aura (classic migraine), in its complete form with slowly progressive visual aura, is virtually never caused by an organic process. A question is frequently raised as to the possibility of arteriovenous malformation.  While headaches may indeed be present with arteriovenous malformation, such vascular lesions more commonly present as subarachnoid hemorrhage or seizure.  In a review of occipital lobe arteriovenous malformations, Troost and Newton⁷ determined that the characteristic visual phenomena represent occipital epilepsy, and the nonalternating, unilateral character of the headache, as well as the history of a seizure, always distinguished these vascular malformations from migraine. Rarely, an arteriovenous malformation may produce clinical symptomatology, which in a single episode is indistinguishable from an episode of classic migraine.⁷³  The invariant nature of the attack, lack of response to therapy, and presence of abnormality on examination, such as a cranial bruit, should lead to additional diagnostic studies in these unusual patients.  A normal physical examination, family history, and response to therapy should eliminate the need to perform neuroradiologic studies in the vast majority of patients with migraine. 

Common, classic, and complicated migraine may be precipitated by trauma.  If the typical clinical pattern of one of the migraine syndromes follows head trauma, other additional causes such as subdural hematoma need not be sought.  Complicated migraine can present some of the most difficult diagnostic problems, particularly in the absence of    prior episodes or family history.  The acute onset of neurologic dysfunction and headache in this setting must always be regarded initially as caused by another process, such as cerebrovascular disease or rapidly growing tumor, and must be fully investigated.  Again the prior history of uncomplicated common or classic migraine may lessen the suspicion of another process in a given individual. 

Ophthalmoplegic “migraine” should be diagnosed only in the  typical clinical setting described in the previous section:  a young individual with history of recurrent ophthalmoplegic episodes or known migraine.  Sudden oculomotor nerve palsy associated with previous chronic headache, or with new acute severe headache, should be considered caused by aneurysm until proved otherwise.  With aneurysm, the history is not one of recurrent episodes of ophthalmoplegia with full recovery.  Occasionally other congenital vascular anomalies, meningeal inflammation, or neoplastic disease may produce painful ophthalmoplegia. Diabetic oculomotor palsy usually occurs in older individuals with diabetes, spares the pupil, and is rarely recurrent. Sphenoid sinus mucocele may present as a recurrent headache and third nerve palsy;²³⁶ radiologic studies should clarify the diagnostic dilemma.  

Cranial nerve abnormality other than oculosympathetic paresis in a patient with "cluster" headache should alert the physician to an intracranial mass lesion (Rader paratrigeminal neuralgia, type 1).  Persistent localized pain most often makes this cluster atypical and points to a different etiology. 

In general, a  knowledge of the different headache varieties other than migraine and a careful history and examination will lead to the appropriate diagnosis. 

 

 

 

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