When a women enter an ophthalmologist’s office complaining of headaches with sudden visual problems, the physician must be aware that these symptoms can be indicators of some neurological conditions that target women. The common eye complaints may be pain, double vision, redness or visual loss.
Ophthalmologists are often the first physicians to see patients who are experiencing migraines or the onset of multiple sclerosis.
One neurological disorder which often presents with visual symptoms initially in women is multiple sclerosis. They present first to an ophthalmologist because they notice their loss of vision from optic neuritis or double vision due to inflammation.
The initial signs of multiple sclerosis include monocular vision loss associated with pain on eye movement, diplopia, oscillopsia (objects appear to oscillate), nystagmus, dorsal midbrain syndrome and homonymous hemianopia. A small percentage of patients present with pars planitis, perivenous sheathing or uveitis.
An examination may show visual acuity loss, relative afferent pupillary defect or visual field defect, and the patient could have optic disc oedema.
Anyone with optic neuritis needs an MRI, both with and without gadolinium to see for brain lesions.
Treatment may include intravenous corticosteroids like Solu-Medrol (methylprednisolone sodium succinate) immunomodulating agents, and symptomatic treatment of spasticity, depression and bladder dysfunction.
Oral prednisone not used because the Optic Neuritis Treatment Trial showed that patients are more likely to have another attack of optic neuritis if treated with prednisone.
Migraines can occur at any age after puberty, usually starts in the 20s and continue on until 50. Women are more likely to suffer from this vision-affecting headaches, twice as many women have migraines as men.
Many patients with migraines present with visual phenomena or aura, which can range from zigzag lines or aura to fragmented vision or complete visual loss. These types of symptoms are associated with classic migraines. They experience visual images as a part of migraine event, so patients often go to ophthalmologists to understand the nature of the problem. The role of an ophthalmologist is to recognize that it’s a migrainous event and refer the patient to a neurologist.
The location and consistency of the visual loss and pain is very important. Investigate any headache that is always on the same side and doesn’t follow the rules, if the aura takes longer than the typical time or it’s always on the same side or there are visual field defects in between attacks, then go aggressively and look for some other reason for the headache.
There are occasional instances in which visual phenomena will be misinterpreted to be relating to migraine but, in fact, could be related to some other more significant neurological problem. MRI is indicated in such cases. If the patient experiences persistent visual loss without a headache or if the visual phenomena last longer than the typical hour, neuroimaging should be pursued.
Ophthalmoplegic Migraine, a variant accompanied by diplopia and ptosis. It consists of a headache followed by an oculomotor nerve palsy that may last weeks after the pain resolves. It is most likely inflammatory, rather than migrainous.
There is no specific treatment for aura or visual phenomena, the migrainous headaches may be treated by prophylactic or symptomatic therapy. Transient monocular visual loss is often successfully prevented with verapamil.
Thyroid Eye Disease
Thyroid eye disease, also known as Graves’ orbitopathy or Graves’ disease, affects women in their 50s and 60s and may be associated with thyroid abnormalities. It is often heralded by dry eye symptoms.
Patients usually present with eye irritation and other signs and symptoms of dry eyes, including conjunctival injection, diplopia and periocular pain.
An examination shows corneal exposure, conjunctival injection, injection over the extraocular muscle insertions, unilateral or bilateral proptosis, restriction of ocular motility, eyelid retraction, lid lag, lid erythema or oedema.
Patients with orbitopathy of Graves’ disease most typically experience discomfort because of problems on the ocular surface, so they have low-level chronic discomfort of the eye. The eyes become protuberant, causing cosmetic problems.
In the worst cases, inflammation could be so great that the muscles swell and press on the optic nerve, causing visual loss.
If there is no known thyroid disease, patients should be evaluated for it.
In thyroid eye disease, the antibodies that are made to the thyroid gland attack the eye muscles, and the eye muscles get infiltrated with lymphocytes. They are inflamed and they don’t contract, resulting in double vision.
Since it is an autoimmune disease, one can develop the orbitopathy of Graves’ disease with a hyperactive thyroid gland, a hypoactive thyroid gland or a normally functioning thyroid gland, so the two conditions are related but not directly.
Treating the thyroid condition usually has no significant effect on the ophthalmic manifestations. Ophthalmic treatment comes in the form of lubricants and patching to avoid diplopia, along with radiation therapy and orbital decompression surgery.
Corticosteroids are sometimes used, although there is conflicting data regarding their efficacy. Although signs of optic neuropathy are uncommon, all patients in the active phase of the disease should have routine perimetry every few months.
The disorder generally runs 18 months and then stabilizes, but it can leave the patient with dry eyes, permanent disfigurement from lid retraction, lid erythema and proptosis, diplopia and, rarely, visual loss from optic neuropathy.
Giant Cell Arteritis
Giant cell, or temporal, arteritis presents in women 60 or older with symptoms that may lead the patient directly to the ophthalmologist.
Some patients have early visual symptoms, others will seek care with an internist, dentist, psychiatrist or neurologist. The symptoms may be vague, and a high index of suspicion is needed.
Visual symptoms include amaurosis fugax (sudden black outs), diplopia and sudden visual loss from ischemic optic neuropathy. Other symptoms include headaches, jaw claudication, scalp tenderness or necrosis, fever, weight loss, myalgias and arthralgias, malaise and night sweats.
Typical presentation would be a 75-year-old woman who starts having worsening of her arthritis: aches and pains every place. When she chews, her jaw gets tired. She can’t put her shirt on over her head because her scalp is so sensitive. She can’t comb her hair because her scalp hurts so much when she touches it. She has terrible headaches and then starts to have obscurations of her vision.
If the condition is not treated immediately with steroids, the patient can lose vision quickly. If it’s not recognized and treated immediately it can turn a healthy 75-year-old woman into a blind person who needs to be taken care of. They can lose vision in one eye and 5 minutes later lose vision in the other eye.
Start corticosteroids immediately and then check the sedimentation rate, C-reactive protein, complete blood cell count with platelet count and arrange for a temporal artery biopsy to be performed within a week.
A patient complaining of aches and pains, think temporal arteritis. It’s sufficiently common, especially in 80-year-olds. It gets more and more common as one gets older.
Fish out the history by asking, “Does your jaw get tired when you chew? Do you have scalp sensitivity? Do you have headache?’ And if there’s any inkling that they have temporal arteritis, they should be given prednisone immediately and ask questions later because they can lose vision from anterior ischemic optic neuropathy at any time.”
Idiopathic Intracranial Hypertension
Idiopathic intracranial hypertension is primarily a disorder that affects overweight women of childbearing age, although there are atypical cases.
The initial symptoms include headache, short but frequent transient obscurations of vision unilaterally or bilaterally, pulsatile tinnitus, diplopia and photophobia. Other neurologic symptoms include neck and back pain, radicular pain, ataxia and facial palsy.
An examination shows visual acuity loss, visual field defect, such as an enlarged blind spot, generalized constriction, inferonasal loss or central scotoma, and relative afferent pupillary defect if there is an asymmetrical optic neuropathy. Papilledema is the hallmark of this disorder, although it may be subtle or asymmetrical.
It produces headache and swelling of the optic nerves because of the pressure inside of the skull. The swelling of the optic nerves, when it persists for months, can cause a slow and permanent visual loss.
Neuroimaging and lumbar puncture should be done immediately.
Treatment include diuretics, headache treatments, or surgical procedures such as optic nerve sheath fenestration or shunt.
The patient needs to have a regular examination of the visual field and regular examination of the optic nerve because complications, progression of visual loss could occur and the ophthalmologist is well-suited to detect that and then to communicate the results to the neurologist, which may result in a change in medicine or perhaps even recommendation of surgery if visual loss is progressing.
Cerebral Venous Sinus Thrombosis can have an identical presentation to idiopathic intracranial hypertension. Consider that in a women taking oral contraceptives, smokers and women in the peripartum period. There may be an underlying coagulation disorder.