question: What causes the visual disturbances in a migraine?
comment: [imaging studies have revealed changes in blood flow to the brain during ocular migraines and migraine auras. But why this happens and what brings about the spontaneous resolution of ocular migraines and visual migraines remain unknown.]( URL_0 ) I get them. Have looked into it before, and there's just no actual proof of what is going on, that I'm aware of.
passages: Vision disturbances often consist of a scintillating scotoma (an area of partial alteration in the field of vision which flickers and may interfere with a person's ability to read or drive). These typically start near the center of vision and then spread out to the sides with zigzagging lines which have been described as looking like fortifications or walls of a castle. Usually the lines are in black and white but some people also see colored lines. Some people lose part of their field of vision known as hemianopsia while others experience blurring.
   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.
   Retinal migraines are a subclass of optical migraines. Sufferers will experience a scotoma—a patch of vision loss in one eye surrounded by normal vision—for less than one hour before vision returns to normal. Retinal migraines may be accompanied by a throbbing unilateral headache, nausea, or photophobia.
  
  Section::::Not classified in the ICHD-2 under migraine.
  
  Section::::Not classified in the ICHD-2 under migraine.:Acephalgic migraine.
   The role of migraines in Alice in Wonderland syndrome is still not understood, but both vascular and electrical theories have been suggested. For example, visual distortions may be a result of transient, localized ischaemia (an inadequate blood supply to an organ or part of the body) in areas of the visual pathway during migraine attacks. In addition, a spreading wave of depolarization of cells (particularly glial cells) in the cerebral cortex during migraine attacks can eventually activate the trigeminal nerve's regulation of the vascular system. The intense cranial pain during migraines is due to the connection of the trigeminal nerve with the thalamus and thalamic projections onto the sensory cortex. Alice in Wonderland syndrome symptoms can precede, accompany, or replace the typical migraine symptoms.
   The terms "retinal migraine" and "ocular migraine" are often confused with "visual migraine", which is a far-more-common symptom of vision loss, resulting from the aura phase of the common migraine. The aura phase of migraine can occur with or without a headache. Ocular or retinal migraines happen in the eye, so only affect the vision in that eye, while visual migraines occur in the brain, so affect the vision in both eyes together. Visual migraines result from cortical spreading depression and are also commonly termed scintillating scotoma.
  
  Section::::Symptoms.
   BULLET::::- Childhood periodic syndromes that are commonly precursors of migraine include cyclical vomiting (occasional intense periods of vomiting), abdominal migraine (abdominal pain, usually accompanied by nausea), and benign paroxysmal vertigo of childhood (occasional attacks of vertigo).
  
  BULLET::::- Retinal migraine involves migraine headaches accompanied by visual disturbances or even temporary blindness in one eye.
  
  BULLET::::- "Complications of migraine" describe migraine headaches and/or auras that are unusually long or unusually frequent, or associated with a seizure or brain lesion.
   BULLET::::- Multiple sclerosis can cause amaurosis fugax due to a unilateral conduction block, which is a result of demyelination and inflammation of the optic nerve, and "...possibly by defects in synaptic transmission and putative circulating blocking factors."
  
  BULLET::::- Migraine
  
  BULLET::::- Pseudotumor cerebri
  
  BULLET::::- Intracranial tumor
  
  BULLET::::- Psychogenic
  
  Section::::Diagnosis.
   Persisting visual snow can feature as a leading addition to a migraine complication called persistent aura without infarction, commonly referred to as persistent migraine aura (PMA). In other clinical sub-forms of migraine headache may be absent and the migraine aura may not take the typical form of the zigzagged fortification spectrum, but manifests with a large variety of focal neurological symptoms.
   In general, the prognosis for retinal migraine is similar to that of migraine headache with typical aura. As the true incidence of retinal migraine is unknown, it is uncertain whether there is a higher incidence of permanent neuroretinal injury. The visual field data suggests that there is a higher incidence of end arteriolar distribution infarction and a higher incidence of permanent visual field defects in retinal migraine than in clinically manifest cerebral infarctions in migraine with aura. One study suggests that more than half of reported "recurrent" cases of retinal migraine subsequently experienced permanent visual loss in that eye from infarcts, but more recent studies suggest such loss is a relatively rare side effect.
   The medical exam should rule out any underlying causes, such as blood clot, stroke, pituitary tumor, or detached retina. A normal retina exam is consistent with retinal migraine.
  
  Section::::Treatment.
  
  Treatment depends on identifying behavior that triggers migraine such as stress, sleep deprivation, skipped meals, food sensitivities, or specific activities. Medicines used to treat retinal migraines include aspirin, other NSAIDS, and medicines that reduce high blood pressure.
  
  Section::::Prognosis.
   Acephalgic migraine is a neurological syndrome. It is a variant of migraine in which the patient may experience aura symptoms such as scintillating scotoma, nausea, photophobia, hemiparesis and other migraine symptoms but does not experience headache. Acephalgic migraine is also referred to as amigrainous migraine, ocular migraine, ophthalmic migraine or optical migraine, last three being misnomers.
  
  Sufferers of acephalgic migraine are more likely than the general population to develop classical migraine with headache.
   Acephalgic migraine
  
  Acephalgic migraine (also called acephalalgic migraine, migraine aura without headache, amigrainous migraine, isolated visual migraine, and optical migraine) is a neurological syndrome. It is a relatively uncommon variant of migraine in which the patient may experience aura, nausea, photophobia, hemiparesis, and other migraine symptoms, but does not experience headache. It is generally classified as an event fulfilling the conditions of migraine with aura with no (or minimal) headache. It is sometimes distinguished from visual-only migraine aura without headache, also called ocular migraine.
  
  Section::::Symptoms and misdiagnosis.
   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.
  
  Section::::Treatment.
  
  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.
  
  Section::::See also.
  
  BULLET::::- ICHD classification and diagnosis of migraine
   Note also that migraine without aura can be diagnosed even if a patient has before experienced an aura.
  
  One popular theory in migraine pathophysiology is the depolarization theory, which centres around the phenomenon of cortical spreading depression. However, it appears that this theory can not account for migraine without aura. Blood flow imaging has revealed no evidence of this phenomenon, though it has noted some changes in blood flow that are secondary to pain activation, particularly in the brainstem.
   Past research has linked macropsia to migraine. One of these studies was conducted on Japanese adolescents who reported visual episodic illusions with macropsia and showed that illusions are three times more likely to occur in association with migraine. The illusions were most prevalent among girls between the ages of 16 and 18. It is unlikely that macropsia in Japanese adolescents could be due to epileptic seizure since only 0.3% of Japanese adolescents have epilepsy. No evidence of drugs was found, which eliminates the possibility of the macropsia in the adolescents being drug-induced. It is also unlikely for macropsia in adolescent children to be associated with a serious disease. It is usually the macropsia or other visual disturbance which precedes the painful migrainous headaches. The episodes of macropsia can occur as part of the aura in a migraine. These episodes are often brief, lasting only a few minutes. Adolescents who are deemed to have multiple distortions per episode, such as slow motion vision and macropsia, are even more likely to be sufferers of migraine. The macropsia episodes associated with migraine are typically equivalent to the duration of the aura, which can range from moments to 15 minutes. Non-migrainous headaches are not known to be associated with episodic illusions. Even in the absence of a migraine, a fever or a hypnagocic state can provoke visual illusions, which one might claim to be macropsia. A person with macropsia may fail to see the connection between the migraine and the macropsia, since the conditions may not elicit symptoms at the same time. The pathophysiology of the condition is not fully understood, but the timing of some episodic occurrences with the headaches suggests that there is a connection between macropsia and the vasoconstrictive phase of a migraine. The differences in visual phenomena, such as macropsia with slow motion versus macropsia without slow motion, may result from different areas of the brain being affected by migraine.
   In their findings, it was observed that a typical hallucination period was of 5–60 minutes, occurred either before or with the onset of head pain, and typically consisted of an unpleasant odor. It was also noted that phantosmia occurs most commonly among women having a migraine complaint. In their study, prophylactic therapy for headaches helped cure phantosmia in most of the patients.
  
  This finding is consistent with the findings of Schreiber and Calvert in 1986 which also mentioned the olfactory hallucinations before the occurrence of a migraine attack in four of their subjects.
  
  Section::::Case studies.
   Cortical spreading depression, or "spreading depression" according to Leão, is a burst of neuronal activity followed by a period of inactivity, which is seen in those with migraines with an aura. There are a number of explanations for its occurrence, including activation of NMDA receptors leading to calcium entering the cell. After the burst of activity, the blood flow to the cerebral cortex in the area affected is decreased for two to six hours. It is believed that when depolarization travels down the underside of the brain, nerves that sense pain in the head and neck are triggered.
  
  Section::::Pathophysiology.:Pain.
   In addition to visual snow, many of those affected have other types of visual disturbances such as starbursts, increased afterimages, floaters, trails, and many others.
  
  Section::::Signs and symptoms.:Comorbidities.
  
  Migraine and migraine with aura are common comorbidities. However, comorbid migraine worsens some of the additional visual symptoms and tinnitus seen in "visual snow" syndrome. This might bias research studies by patients with migraine being more likely to offer study participation than those without migraine due to having more severe symptoms. In contrast to migraine, comorbidity of typical migraine aura does not appear to worsen symptoms.
   An aura is a transient focal neurological phenomenon that occurs before or during the headache. Auras appear gradually over a number of minutes and generally last less than 60 minutes. Symptoms can be visual, sensory or motor in nature and many people experience more than one. Visual effects occur most frequently; they occur in up to 99% of cases and in more than 50% of cases are not accompanied by sensory or motor effects.
   Section::::Pathophysiology.
  
  Section::::Pathophysiology.:FHM1 ("CACNA1A").
   Ménière's disease - There is an increased prevalence of migraine in patients with Ménière's disease and migraine leads to a greater susceptibility of developing Ménière’s disease. But they can be distinguished. Ménière's disease may go on for days or even years, while migraines typically do not last longer than 24 hours.
  
  Motion sickness is more prevalent in patients with migraine.
   Illusory palinopsia may occur during a migraine aura, as do other diffuse illusory symptoms such as halos around objects, visual snow, dysmetropsia, and oscillopsia. In a rare migraine subtype known as persistent visual aura without infarction, illusory palinopsia symptoms (prolonged indistinct afterimages, light streaking, and visual trailing) persist after the migraine has abated. Alternatively, up to 10% of all migraineurs report of formed afterimages that only last a couple seconds and do not occur with other illusory symptoms. These momentary afterimages appear at a different location in the visual field than the original stimulus, occur a few times per month, and are affected by external light and motion. (variant image perseveration). Migraineurs with these momentary afterimages report significantly fewer migraine headaches than migraineurs without these afterimages (4.3 vs. 14.4 attacks/year). These afterimages probably represent an overlap in hallucinatory and illusory palinopsia. Studying these momentary formed afterimages, in relation to alterations in cortical excitability, could advance our understanding of migraine pathogenesis and mechanisms associated with encoding visual memory.
   In 2000, the German national daily newspaper "Die Welt" published an article about the work of the theoretical physicist Markus Dahlem on the emergence of visual hallucinations during migraine. In the following days and weeks, the scientist received numerous letters asking for more information and many people were willing to provide additional information on their migraine symptoms.
   There are suggestions that visual distortions, such as macropsia, can be associated with cocaine use. Episodes of temporary drug-induced macropsia subside as the chemicals leave the body.
  
  Section::::Causes.:Migraine.
   Retinal migraine is a different disease than scintillating scotoma, which is a visual anomaly caused by spreading depression in the occipital cortex at the back of the brain, not in the eyes nor any component thereof. Unlike in retinal migraine, a scintillating scotoma involves repeated bouts of temporary diminished vision or blindness and affects vision from both eyes, upon which sufferers may see flashes of light, zigzagging patterns, blind spots, or shimmering spots or stars.
  
  Section::::Diagnosis.
  