The first thing to think about is whether this is really a monocular problem?.
If really monocular, then the problem is anterior to the optic chiasm, that is in the optic nerve, orbit, globe or retina. It is an eye problem, not a brain problem.
If not monocular, but the display is in the left side of the visual field of each eye (easily ignored on the right, since the left field OD consists mostly of the nose) then the problem is posterior to the optic chiasm (crossing of the optic nerves) and hence is in the brain.
Much turns on this distinction. To evaluate it, do the following when the patient sees the spots.
The patient should stare at a blank wall (no pattern) when this happens and alternately cover each eye, looking to see whether there are a few spots in the in the left side of the visual field of each eye separately. If so, the problem is retro-chiasmal and, hence, a brain problem, not an eye problem.
If it is really only the visual field of the left eye alone that is involved, then it is an eye/orbit problem.
Monocular blurred vision in a young woman with asymmetric pupils may be Aide’s syndrome. The typical patient presents with monocular blurred vision, because depth of field is constricted as a result of an pupillary dysfunction. The key is in the pupil examination. The left pupil reaction may be sluggish (tonic) compared to the right. The novice general neurologist might easily confuse this with an RAPD (relatively afferent pupillary defect) and suspect an optic neuropathy, of which optic neuritis is only one of many. However, this is not an optic neuropathy and hence there is nothing to be found by the million dollar splashing around.
Monocular spots may be “floaters” or little vitreal hemorrhages which move with the eye, but lag behind the eye movement a little, giving the “drifing” impression and, hence. the name. These should not occur in young people.
The next question is whether the spots and light, colored or brown/black. The former are “positive” visual phenomena. The latter are negative phenomena.
Positive visual phenomena that occur as evanescent, very brief sparks (like from a welder’s torch) are called phosphenes and denote irritation of the retinal ganglion cell nerve fiber layer in the eye. These are usually white or yellow.
Positive visual phenomena that occur as a kaleidoscopic pattern of bars of light with angles of about 60 degrees between the bars and the bars arranged in an arc or semi-circle that moves out slowly in the visual field over 20 minutes is called a teichopsia or “fortification spectra.” It is a migraine auar. BVecause it originates from the visual cortex it is usually binocular (seen in each eye), although the patient may ignore it in the nasal field of one eye. (It will be in the same side of the visual field of each eye). There are no monocular migraine auras.
Positive visual phenomena which are lava-light like multicolored moving blobs suggest primary visual cortex pathology.
Positive visual phenomena which are paisley patterns, “fields of flowers,” “fields of grass” displays are also visual cortex in origin although primary nearly visual association cortex may be involved as well,
Multiple reproductions of the same visual target arranged in an arc or circle (as in 6 – 8 television sets all arranged in an arc is called cerebral polyopia and is thought to be inferior temporal gyrus (temporal lobe) visual monomodal association cortex dysfunction.
Perseveration of the visual target in time, as with multiple, progressively more faint after images of the visual target (like mouse tracks on the computer) is cerebral Palinopsia and is also a temporal lobe visual association cortical dysfunction.
It is difficult to tie facial sensation or clumsiness or ataxia into a primary visual pathway lesion with one exception. The primary visual cortex (in most people), inferior medial thalamus, brainstem and cerebellum are all served by the vertebral-basilar vascular system. So vertebrobasilar vascular insufficiency might give the assortment of problems (trigeminal, cerebellar, visual) that you describe.
One must also consider the facts that there are no obvious structural or anatomic lesions on imaging. These might be missed, but I shall put aside this possibility, since there have been multiple different studies. Taking it as given that there is no structural abnormality, then attention must turn to those things that might not have a imaging footprint. These are:
1. Mitochondrial disease (Kearn-Sayers and the like) particularly in the orbit
2. Orbital pseudo-tumor (unless dedicated fat suppressed orbital MRI was obtained)
3. Cavernous sinus pseudo-tumor
4. Occipital seizure
5. Inferior temporal gyrus seizure
6. Genetic neurodegenerative disease, such as one of the 27 SCA syndromes (spinal cerebellar atrophy)
7. Genetic neurodegenerative disease, such as frontotemporal dementia, Lewy body disease or the like
8. Intoxication
9. Poisoning
10. Pseudo-tumor cerebri
11. Intracranial hypotension syndrome
12. Complicated migraine headache
13. Superficial hemosiderosis of the central nervous system
14. Lupus cerebritis
15. Early Hashimoto’s encephalitis
16. Peduncular hallucinosis
17. Hypothalamic hamartoma
18. Many others
I hope this helps.
Robert W Jensen, MD, JD,. FCLM
Associate Professor of Neuro-Ophthalmology & Neuro-Otology
University of Kansas School of Medicine – Wichita Campus
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