In essence, these are collections of symptoms, that are called "migraines", by the International Headache Society. Of course, there are many other central nervous system disturbances associated with the same genes are not called migraine. This is a problem. Classic migraine : Migraine headache with aura loss of vision or other visual symptoms, paresthesias, motor dysfunction precedes the throbbing headache. An electrical change -- cortical spreading depression within the occipital cortex -- generates most visual areas as well as some sensory symptoms.
An example of an aura drawn by one of my patients is here. Common migraine : Migraine headache without aura. Vertebrobasilar migraine : headache accompanied by dizziness or ataxia, hearing symptoms other than phonophobia , nausea and vomiting, and sometimes loss of consciousness.
See related page on " Migraine associated Vertigo ". Transient monocular blindness can occur in migraine, particularly those associated with elevated antiphospholipid antibodies or lupus anticoagulant Donder et al, ; Levine et al, However recent work Donder et al, suggests that among patients with lupus, no significant relation can be found between transient monocular blindness and the presence of APA or livedo reticularis.
This observation suggests that APA may be a symptom of lupus rather than a cause of transient monocular blindness. Antiphospholipid syndromes are also associated with neuropsychiatric disease Afeltra et al , recurrent miscarriages, and a reticular rash on the legs.
Acephalgic migraine : Aura without headache. This diagnosis is generally made when persons who have headache and aura, also have aura without headache. This content does not have an English version.
This content does not have an Arabic version. Overview A migraine is a headache that can cause severe throbbing pain or a pulsing sensation, usually on one side of the head.
Request an Appointment at Mayo Clinic. Mayo Clinic Minute Weathering migraines. Share on: Facebook Twitter. Show references Cutrer FM, et al. Pathophysiology, clinical manifestations, and diagnosis of migraine in adults. Accessed Jan. Migraine information page. National Institute of Neurological Disorders and Stroke. Headache: Hope through research. Accessed Feb. Smith JH, et al. Acute treatment of migraine in adults. Simon RP, et al. In: Clinical Neurology. McGraw Hill; Ha H, et al. Migraine headache prophylaxis.
American Family Physician. Kissoon NR expert opinion. Mayo Clinic. March 16, Preventive treatment of episodic migraine in adults. Kleinman K, et al. In: Harriet Lane Handbook. Elsevier; Taylor FR. Its nocturnal occurrence is thought to be related to circadian activation of certain neurotransmitters during sleep, which are known to trigger a migraine attack.
The neurologic examination in between attacks is nonfocal. Ictally, hemiparesis, ophthalmoplegia, or altered consciousness may be observed.
Abnormalities of oculomotor nerve with pupillary involvement are seen in ophthalmoplegic migraine, followed by the abducens, and less commonly trochlear nerve palsy. Children with abdominal migraine or cyclic vomiting may show subtle clumsiness, attention deficit, or developmental delay.
In migrainous infarction, some form of neurologic deficit with abnormal neuroimaging is present. Rarely, when patients with retinal migraine are evaluated and examined during an attack of visual loss, optic pallor or narrowing of the retinal vessels can be seen.
Neuroimaging CT, MRI is indicated when the patient presents with the first attack of a focal neurologic deficit or altered mental status, or when focal findings persist between attacks. Neuroimaging studies are frequently obtained to exclude other acute causes of the symptoms and to exclude migrainous infarction in patients with persistent aura.
MR imaging of the brain and MR Angiogram of the circle of Willis is indicated in ophthalmoplegic migraine to exclude posterior fossa or orbital pathologies associated with ophthalmoplegia. Abnormal enhancement on MRI and enlargement of the cisternal portion of the oculomotor nerve, have been reported. Further assessment may include a CT angiogram or lumbar puncture. The yield for diagnostic testing in basilar migraine is low.
Transient abnormalities on CT scan and MRI have been reported during or immediately following attacks. SPECT studies suggest decreased regional cerebral blood flow in the posterior circulation in basilar migraine during attacks, but transcranial Doppler studies have not revealed changes in blood flow velocities. Invasive testing in children with periodic syndromes with a strong family history of migraine is unnecessary. A high-resolution MRI and magnetic resonance angiography MRA are indicated in suspicious cases in the absence of supportive family history.
In retinal migraine, it is important to rule out eye disease or vascular causes, especially when risk factors for arteriosclerosis exist. Fluorescein or cerebral angiographies are rarely necessary. Hypercoagulability workup and sedimentation rate may be useful in excluding other coagulation disorders associated with retinal vasculopathy. EEG is considered in conditions where seizure disorders need to be excluded, such as migraine-triggered seizure, and in patients with recurrent episodes of confusion.
EEG generally does not offer additional information in migraine patients. In general, nonspecific interictal EEG abnormalities, including epileptiform activity are reported with higher frequency in migraine patients during or immediately after an episode, with slowing in focal or generalized patterns, and occipital spike-wave complexes.
Continuous ambulatory or video EEG may be useful in patients with episodic confusion or recurrent focal neurologic deficits to exclude partial seizures or nonconvulsive status epilepti. Genetic testing may also be performed for other conditions associated with migraine such as CADASIL, an autosomal dominant disorder in which patients may present with migraine, multiple subcortical strokes, and dementia in early adulthood.
In children with cyclic vomiting, a serum lactate level is helpful in excluding mitochondrial disorders. Other tests including, upper and lower gastrointestinal series and vagal autonomic function testing, are rarely indicated.
More recently, functional neuroimaging studies during and immediately after an attack of migraine have demonstrated abnormalities of perfusion and have helped in understanding the pathophysiology of auras.
The first step in treatment is to establish the diagnosis. Once the syndromes are recognized, MVs respond to typical migraine preventive medications. Treatment is divided into eliminating particular triggers, acute management of the specific attack, and long-term preventive approach. Patients should follow risk factor modifications including smoking cessation, and they should avoid the use of hormonal replacement therapy and birth control pills, all of which could potentially increase the risk of hypercoagulability in migraine patients.
In hemiplegic migraine, acute treatment options include antiemetics, nonsteroidal anti-inflammatory drugs, and nonnarcotic pain relievers. Triptans and ergotamine preparations are contraindicated because of their potential vasoconstrictive effects. Prophylactic treatment is generally warranted because of the severity of the attacks. No data are available to support the use of any particular antimigraine agent. Beta-blockers, low-dose tricyclics, anticonvulsants, and calcium channel blockers can be administered.
Acetazolamide has been frequently prescribed to patients with hemiplegic migraine, but its benefit in decreasing the frequency or severity of the attacks is questionable. No data support the use of antiplatelet therapy to decrease the risk of stroke. In ophthalmoplegic migraine, prednisone has been used with mixed results. The data on the benefit of prophylactic therapy with beta-blockers, such as propranolol are anecdotal.
In retinal migraine, vasoconstrictive agents such as triptans and ergots should be avoided. The use of prophylactic therapy is also anecdotal; when considered, calcium channel blockers are preferred.
In migraine-triggered seizures, antiepileptic agents are drugs of choice because of their dual benefit in migraine prevention and seizure control In childhood periodic vomiting syndrome, early use of intravenous fluids containing adequate glucose to prevent a catabolic state and analgesics may abort the attack.
Some patients respond to the triptans or ergotamine classes of medication. Antiemetic drugs are usually not effective, but ondansetron may be more efficacious given its central mechanism of action. Preventive medications such as cyproheptadine and tricyclic antidepressants are preferred in children. Abdominal migraine symptoms are usually relieved with sleep. Antiemetics may help aborting an acute attack.
For chronic prevention, low doses of tricyclic antidepressants and flunarizine, a calcium channel blocker, are effective. Other migraine prevention medications are occasionally of some benefit. Triptans, ergots and dihydroergotamine are contraindicated in patients with migrainous infarction. These patients may respond to nonsteroidal anti-inflammatory drugs NSAIDs , antiemetics, and non-narcotic pain relievers.
Prophylactic therapy is recommended, with tricyclics, beta-blockers, calcium channel blockers, or antiepileptic drugs. Long-term antiplatelet therapy is indicated in patients with migrainous infarction. Patients with vertiginous migraine rarely respond to migraine prophylactic therapy. Anecdotal data are available on the benefit of verapamil, a calcium channel blocker and amitriptyline, a tricyclic antidepressant, because of their anticholinergic properties, which may help control the vertigo.
Additionally, non pharmacological techniques enables the patient higher responsibility and self-efficacy in coping with migraine. Counselling, relaxation training, biofeedback and cognitive-behavioural treatments are employed. In case of headache in children, behavioural therapy should be the method of first choice.
Migraine Variants are important to recognise in practice. Awareness leads to correct diagnosis. Investigations are often necessary to rule out other closely similar neurological disorders. Most variants respond well to treatment with antimigraine prophylaxis.
If diagnosed correctly, treatment response is always satisfying. Previous Previous Next Next. Article Submission. Remember me. Register Now. Past Issue: April - Dark mode.
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