Prenatal screening is not typically done for FHM, however it may be performed if requested. As penetrance is high, individuals found to carry mutations should be expected to develop signs of FHM at some point in life.

"See the equivalent section in the main migraine article."

People with FHM are encouraged to avoid activities that may trigger their attacks. Minor head trauma is a common attack precipitant, so FHM sufferers should avoid contact sports. Acetazolamide or standard drugs are often used to treat attacks, though those leading to vasoconstriction should be avoided due to the risk of stroke.

Prenatal screening is not typically done for FHM, however it may be performed if requested. As penetrance is high, individuals found to carry mutations should be expected to develop signs of FHM at some point in life.

Diagnosis of FHM is made according to the following criteria:

- Two attacks of each of the following:

- At least one close (first or second degree) relative with FHM

- No other likely cause

Sporadic forms follow the same diagnostic criteria, with the exception of family history.

In all cases, family and patient history is used for diagnosis. Brain imaging techniques, such as MRI, CAT scans and SPECT, are used to look for signs of other familial conditions such as CADASIL or mitochondrial disease, and for evidence of cerebellar degeneration. With the discovery of causative genes, genetic sequencing can also be used to verify diagnosis (though not all genetic loci are known).

MAV is not recognized as a distinct diagnostic entity. Lembert and Neuhauser propose criteria for definite and probable migraine-associated vertigo.

A diagnosis of "definite migraine-associated vertigo" includes a case history of:

- episodic vestibular symptoms of at least moderate severity;

- current or previous history of migraine according to the 2004 "International Classification of Headache Disorders";

- one of the following migrainous symptoms during two or more attacks of vertigo: migrainous headache, photophobia, phonophobia, visual or other auras; and

- other causes ruled out by appropriate investigations.

A diagnosis of "probable migraine-associated vertigo" includes a case history of episodic vestibular symptoms of at least moderate severity and one of the following:

- current or previous history of migraine according to the 2004 "International Classification of Headache Disorders";

- migrainous symptoms during vestibular symptoms;

- migraine precipitants of vertigo in more than 50% of attacks, such as food triggers, sleep irregularities, or hormonal change;

- response to migraine medications in more than 50% of attacks; and

- other causes ruled out by appropriate investigations.

Note that, in both of the above criteria, headache is not required to make the diagnosis of migraine-associated vertigo.

They add that, in patients with a clear-cut history, no vestibular tests are required. Other historical criteria which are helpful in making the diagnosis of migraine-associated vertigo are vertiginous symptoms throughout the patient’s entire life, a long history of motion intolerance, sensitivity to environmental stimuli, illusions of motion of the environment, and vertigo that awakens the patient.

Treatment of migraine-associated vertigo is the same as the treatment for migraine in general.

Cluster headache may be misdiagnosed as migraine or sinusitis. Other types of headache are sometimes mistaken for, or may mimic closely, CH. Incorrect terms like "cluster migraine" confuse headache types, confound differential diagnosis and are often the cause of unnecessary diagnostic delay, ultimately delaying appropriate specialist treatment.

Headaches that may be confused with CH include:

- Chronic paroxysmal hemicrania (CPH) is a unilateral headache condition, without the male predominance usually seen in CH. Paroxysmal hemicrania may also be episodic but the episodes of pain seen in CPH are usually shorter than those seen with cluster headaches. CPH typically responds "absolutely" to treatment with the anti-inflammatory drug indomethacin where in most cases CH typically shows no positive indomethacin response, making "Indomethacin response" an important diagnostic tool for specialist practitioners seeking correct differential diagnosis between the conditions.

- Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT) is a headache syndrome belonging to the group of TACs.

- Trigeminal neuralgia is a unilateral headache syndrome, or "cluster-like" headache.

Cluster headaches are often misdiagnosed, mismanaged, or undiagnosed for many years; they may be confused with migraine, "cluster-like" headache (or mimics), CH subtypes, other TACs ( trigeminal autonomic cephalalgias), or other types of primary or secondary headache syndrome. Cluster-like head pain may be diagnosed as secondary headache rather than cluster headache.

A detailed oral history aids practitioners in correct differential diagnosis, as there are no confirmatory tests for CH. A headache diary can be useful in tracking when and where pain occurs, how severe it is, and how long the pain lasts. A record of coping strategies used may help distinguish between headache type; data on frequency, severity and duration of headache attacks are a necessary tool for initial and correct differential diagnosis in headache conditions.

Correct diagnosis presents a challenge as the first CH attack may present where staff are not trained in the diagnosis of rare or complex chronic disease. Although experienced ER staff are sometimes trained to detect headache types, CH attacks themselves are not directly life-threatening, they are linked to an increased risk of suicide.

Individuals with CH typically experience diagnostic delay before correct diagnosis. People are often misdiagnosed due to reported neck, tooth, jaw, and sinus symptoms and may unnecessarily endure many years of referral to ear, nose and throat (ENT) specialists for investigation of sinuses; dentists for tooth assessment; chiropractors and manipulative therapists for treatment; or psychiatrists, psychologists and other medical disciplines before their headaches are correctly diagnosed. Under-recognition of CH by health care professionals is reflected in consistent findings in Europe and the United States that the average time to diagnosis is around seven years. Medical students receive little training in differential diagnoses and management of headaches.

MRI features can be suggestive of cortical hyper intensity and edema.

Prevalence is estimated to be 0.005%. The age of onset has been found to be under 15 years in 40% of cases while it is between 10 and 14 years in one third of the cases. Females outnumber males, 4 to 1. Only 3% have attacks after age 52.

Preventive treatments of migraines include medications, nutritional supplements, lifestyle alterations, and surgery. Prevention is recommended in those who have headaches more than two days a week, cannot tolerate the medications used to treat acute attacks, or those with severe attacks that are not easily controlled.

The goal is to reduce the frequency, painfulness, and/or duration of migraines, and to increase the effectiveness of abortive therapy. Another reason for prevention is to avoid medication overuse headache. This is a common problem and can result in chronic daily headache.

The diagnosis of a migraine is based on signs and symptoms. Neuroimaging tests are not necessary to diagnose migraine, but may be used to find other causes of headaches in those whose examination and history do not confirm a migraine diagnosis. It is believed that a substantial number of people with the condition remain undiagnosed.

The diagnosis of migraine without aura, according to the International Headache Society, can be made according to the following criteria, the "5, 4, 3, 2, 1 criteria":

- Five or more attacks—for migraine "with" aura, two attacks are sufficient for diagnosis.

- Four hours to three days in duration

- Two or more of the following:

- Unilateral (affecting half the head);

- Pulsating;

- Moderate or severe pain intensity;

- Worsened by or causing avoidance of routine physical activity

- One or more of the following:

- Nausea and/or vomiting;

- Sensitivity to both light (photophobia) and sound (phonophobia)

If someone experiences two of the following: photophobia, nausea, or inability to work or study for a day, the diagnosis is more likely. In those with four out of five of the following: pulsating headache, duration of 4–72 hours, pain on one side of the head, nausea, or symptoms that interfere with the person's life, the probability that this is a migraine is 92%. In those with fewer than three of these symptoms the probability is 17%.

All people who present with red flags indicating a dangerous secondary headache should receive neuroimaging. The best form of neuroimaging for these headaches is controversial. Non-contrast computerized tomography (CT) scan is usually the first step in head imaging as it is readily available in Emergency Departments and hospitals and is cheaper than MRI. Non-contrast CT is best for identifying an acute head bleed. Magnetic Resonance Imaging (MRI) is best for brain tumors and problems in the posterior fossa, or back of the brain. MRI is more sensitive for identifying intracranial problems, however it can pick up brain abnormalities that are not relevant to the person's headaches.

The American College of Radiology recommends the following imaging tests for different specific situations:

The US Headache Consortium has guidelines for neuroimaging of non-acute headaches. Most old, chronic headaches do not require neuroimaging. If a person has the characteristic symptoms of a migraine, neuroimaging is not needed as it is very unlikely the person has an intracranial abnormality. If the person has neurological findings, such as weakness, on exam, neuroimaging may be considered.

The prevention and treatment of acephalgic migraine is broadly the same as for classical migraine, but the symptoms are usually less severe than those of classic migraine, so treatment is less likely to be required.

As of 1993 only approximately 30 people with AHC had been described in scientific literature. Due to the rarity and complexity of AHC, it is not unusual for the initial diagnosis to be incorrect, or for diagnosis to be delayed for several months after the initial symptoms become apparent. The average age of diagnosis is just over 36 months. Diagnosis of AHC is not only difficult because of its rarity, but because there is no diagnostic test, making this a diagnosis of exclusion. There are several generally accepted criteria which define this disorder, however other conditions with a similar presentation, such as HSV encephalitis, must first be ruled out. Due to these diagnostic difficulties, it is possible that the commonness of the disease is underestimated.

The following descriptions are commonly used in the diagnosis of AHC. The initial four criteria for classifying AHC were that it begins before 18 months of age, includes attacks of both hemiplegia on either side of the body, as well as other autonomic problems such as involuntary eye movement (episodic monocular nystagmus), improper eye alignment, choreoathetosis, and sustained muscle contractions (dystonia). Finally, patients suffer from intellectual disabilities, delayed development, and other neurological abnormalities. These diagnostic criteria were updated in 1993 to include the fact that all of these symptoms dissipate immediately upon sleeping. Diagnostic criteria were also expanded to include episodes of bilateral hemiplegia which shifted from one side of the body to the other.

Recent criteria have been proposed for screening for AHC early, in order to improve the diagnostic timeline. These screening criteria include focal or unilateral paroxysmal dystonia in the first 6 months of life, as well as the possibility of flaccid hemiplegia either with or separate from these symptoms. Paroxysmal ocular movements should also be considered, and these should include both binocular and monocular symptoms which show in the first 3 months of life.

Although the original Silberstein–Lipton criteria and the original description by Vanast make no suggestion for the exclusion of migrainous features in NDPH, the current ICHD criteria exclude patients with migrainous features. When migraine features are present, classification thus becomes problematic.

It has been reported that migraine symptoms may be present in over 50% of NDPH patients. The current criteria definition thus excludes more than half of patients with new onset of daily headache. This exclusion due to migrainous features could have adverse scientific, diagnostic, and treatment consequences.

One proposal for reclassification of the criteria is from a study conducted on retrospective analysis of the records of 1348 patients regularly treated at the headache clinic of the Department of Neurology of Santa Casa de São Paulo, Brazil, and would be the following subdivision: NDPH with migraine features and without migraine features that would allow the inclusion of all individuals present who has a daily and persistent headache from the beginning.

Another proposed reclassification of the criteria is from a study conducted as a retrospective chart review of patients seen at the Headache Center at Montefiore Medical Center in Bronx, New York, from September 2005 to April 2009. The revised criteria for NDPH definition does not exclude migraine features (NDPH-R), and three subdivisions were created and described based on prognosis: Persisting, remitting, and relapsing–remitting. Additionally, this revised criteria would not include parts C or D currently required by the ICHD diagnostic criteria for NDPH.

Most patients have persistent headaches, although about 15% will remit, and 8% will have a relapsing-remitting type. It is not infrequent for NDPH to be an intractable headache disorder that is unresponsive to standard headache therapies.

THS is usually diagnosed via exclusion, and as such a vast amount of laboratory tests are required to rule out other causes of the patient's symptoms. These tests include a complete blood count, thyroid function tests and serum protein electrophoresis. Studies of cerebrospinal fluid may also be beneficial in distinguishing between THS and conditions with similar signs and symptoms.

MRI scans of the brain and orbit with and without contrast, magnetic resonance angiography or digital subtraction angiography and a CT scan of the brain and orbit with and without contrast may all be useful in detecting inflammatory changes in the cavernous sinus, superior orbital fissure and/or orbital apex. Inflammatory change of the orbit on cross sectional imaging in the absence of cranial nerve palsy is described by the more benign and general nomenclature of orbital pseudotumor.

Sometimes a biopsy may need to be obtained to confirm the diagnosis, as it is useful in ruling out a neoplasm.

Differentials to consider when diagnosing THS include craniopharyngioma, migraine and meningioma.

Because epileptic seizures may occur with a side effect that resembles migraine aura, it is complicated to diagnose whether a patient is having a normal epileptic episode or if it is a true migraine that is then being followed by a seizure, which would be a true sign of migralepsy. Many neurological symptoms can only be expressed by the patient, who can confuse different feelings, especially when the symptoms of a migraine are extremely similar to that of a seizure. Thus, many physicians are reluctant to consider migralepsy to be a true condition, considering its rarity, and those that do believe in it are prone to over-diagnose it, leading to more problems in terms of finding the truth of the condition.

However, it has been found that EEG scans have been able to differentiate between migraine auras and auras related to epilepsy. It has generally been seen that EEG scans are not as helpful in determining facets of migraines as they are with epilepsy. Though they are able to work in determining the starting and ending points of migraines and the overlap of epileptic episodes during or after them, even if the scans are still lacking in considerable necessary data and confusing results. EEG scans have been able to observe seizures that occur in between the aura and headache phase of migraines and such occurrences have been termed intercalated seizures.

Acephalgic migraines can occur in individuals of any age. Some individuals, more commonly male, only experience acephalgic migraine, but frequently patients also experience migraine with headache. Generally, the condition is more than twice as likely to occur in females than males. Pediatric acephalgic migraines are listed along with other childhood periodic syndromes by W.A. Al-Twaijri and M.I. Shevell as "migraine equivalents" (although not listed as such in the "International Classification of Headache Disorders"), which can be good predictors of the future development of typical migraines. Individuals who experience acephalgic migraines in childhood are highly likely to develop typical migraines as they grow older. Among women, incidents of acephalgic migraine increase during perimenopause.

Scintillating scotoma is the most common symptom which usually happens concurrently with Expanding Fortification Spectra. Also frequently reported is monocular blindness. Acephalgic migraines typically do not persist more than a few hours and may last for as little as 15 seconds. On rare occasions, they may continue for up to two days.

Acephalgic migraines may resemble transient ischemic attacks or, when longer in duration, stroke. The concurrence of other symptoms such as photophobia and nausea can help in determining the proper diagnosis. Occasionally, patients with acephalgic migraine are misdiagnosed as suffering epilepsy with visual seizures, but the reverse misdiagnosis is more common.

There is no known prevention of spinocerebellar ataxia. Those who are believed to be at risk can have genetic sequencing of known SCA loci performed to confirm inheritance of the disorder.

Benign paroxysmal torticollis disappears in the early years of life with no medical intervention.

However, some cases of benign paroxysmal torticollis cases can evolve into benign paroxysmal vertigo of childhood, migrainous vertigo or typical migraines.

No known treatment for BPT currently exists. However, the condition it is self-limiting and resolves after about eighteen months.

Benign paroxysmal vertigo of childhood is an uncommon neurological disorder which presents with recurrent episodes of dizziness. The presentation is usually between the ages of 2 years and 7 years of age and is characterised by short episodes of vertigo of sudden onset when the child appears distressed and unwell. The child may cling to something or someone for support. The episode lasts only minutes and resolves suddenly and completely. It is a self-limiting condition and usually resolves after about eighteen months, although many go on to experience migrainous vertigo (or vertiginous migraine) when older.

Benign paroxysmal vertigo of childhood is a migrainous phenomenon with more than 50% of those affected having a family history of migraines affecting a first-degree relative. It has no relationship to benign paroxysmal positional vertigo which is a different condition entirely.