 is Anna Neufallon. I think most of you have met me to date. I'm the new neurophthalmology fellow, not so new anymore I guess, but still new to some. So I'm gonna talk about frontal lobe pathology and what it does to the eyeballs. So I'm gonna start with a briefcase presentation and then we'll review the relevant anatomy and some literature and then I'll conclude with three important takeaway points that I think everyone should remember from my brief presentation today. So this is a woman we saw in August this year. She is a 66-year-old and was referred to neurophthalmology because of suspected non-autoritic ischemic optic neuropathy and she describes it as a kind of gradual onset vision loss over six months or so and she denies having any other symptoms like GCA symptoms or headaches or constitutional symptoms. Relevant history includes the fact that she did have cancer uterine cancer in 2012 which was treated successfully and she also has this very severe depression and she even required hospitalization for it two months prior to seeing us and she was admitted for two weeks because of it. These are her medications so she's on an exanalytic medication and an antidepressant for her depression and these are her examination findings. So first of all when when we entered the room she looked very apathetic, very uninterested in the testing, kind of falling asleep during the testing so she had a friend there with her who was helping her kind of through this and through the exam so keeping that in mind you know the exam and the visual field testing was somewhat unreliable but we were able to get her to 2200 on the right but this was very kind of eccentric viewing forcing her to to get to that line and then the left she was about 22 over 40. Her pressures were normal but she did have a large relative afferent pupillary defect on the right and a collivision deficiency on the right which was consistent with optic neuropathy. She had bilateral ptosis with MRD1 of about one millimeter and on anterior segment the only pathology was really some mild to moderate cataract changes. A dilated fundus examination showed temporal disc pallor on the right and a disc at risk and on the left the nerve looked healthy but also had the appearance of a tight optic nerve with a disc at risk. Her dilated exam and peripheral retina were normal. So these are her visual fields as I mentioned there were somewhat unreliable but what I want to draw your attention to is the fact that the right visual field has this global depression and on the left there's a suggestion of a superior arcuate defect and there is a visual field deficit kind of infrotemporal on that left eye because you don't really have the right eye to help you to guide whether this is indeed a neurological visual field or not. You kind of have to presume that it is either a bi-temporal visual field deficit or a homonymous visual field deficit which we can't really tell from the fields. I don't have color photos but these are the OCT images and it kind of gives you the impression that the discs are not cupped they don't see much cupping there and if we superimpose the retinal nerve fibularis scan on top this is the pattern of RNFL loss and you can see that the majority of the loss is actually in the temporal area and maybe some inferior nasal and on the left it was normal. So what's next? Is this NAON? Could we just assume that and maybe look for risk factors and just let her be? Well I think there are some definite red flags in this patient and specifically she's a woman in her 60s. She has this gradual onset rather than kind of a sudden realization of vision loss, a sudden loss of vision. She has a possible neurologic deficit with that inferior temporal deficit on the left so we were of course concerned about possible compression or neurologic pathology so we proceeded with imaging. So I don't think I need to use my pointer here to point out the pathology but you can see that in her frontal lobe there's a large mass. These are the axial and curl T1 MR images post gastrointestinal suppression and this mass measured about 7 by 7 by 5 centimeters in size and I'm not quite seeing in this image but it was compressing the right pre-chiasmic optic nerve and at the end of the distal optic canal and some mild compression of the optic chiasm. So immediately as we saw the scan we sent this woman to the emergency room there's a lot of vasogenic edema around the lesion so she was admitted and operated on. The pathology came back as meningioma who grade 1. So let us talk briefly about frontal lobinatomy and how that relates to the eye. First of all visual pathways take up about a third of the overall brain volume so I think ophthalmologists in general should and do have a good understanding of how neurological lesions cause visual pathology. However I think frontal lobe is often forgotten as a possible site of pathology for the visual system. So frontal lobe contains about 30% of the cerebral volume of the brain and as I mentioned we kind of rarely think about it as a site for lesions that cause visual pathology. So to briefly review the the anatomy here we have the the Broca's area which is present in the dominant hemisphere which is responsible for speech. You have the prefrontal cortex which is your personality and executive behaviors functional area. We have your precentral gyres which is your primary motor cortex and you have some supplementary motor areas which are responsible for motor planning. But most importantly I think and often again forgotten is this area here called the frontal eye fields that we'll we'll discuss in in a minute as well. So in terms of general pathology in the frontal lobe the most common benign and malignant is meningiomas and they're 10 to 50% of all benign frontal lobe tumors and on the malignant side those are gliomas and they're 70% of all malignant brain tumors in the frontal lobe. And I briefly wanted to mention some psychiatric presentations of the frontal lobe tumors which are important to keep in mind and I think you can look at it both ways. You can look at all the patients that present with psychiatric illness and see how many of them have frontal pathology in terms of masses or otherwise. So if you look at all acute psychiatric presentations the brain tumors are present in 0.3% so not too common that was published quite quite a few years ago but even in the new publications this is still in keeping with those numbers. If you look at all the hospitalized psychiatric patients that number is about 1 in 200 which is pretty close to the original numbers. However if you think about the normal population and the rate of incidental findings there it's about 20% of that of the normal population. Now if you flip it around and look at the patients who are known to have frontal lobe pathology and frontal lobe tumors actually 60 to 90% of them have psychiatric illnesses and to put that in perspective if you look at all the patients with brain pathology about 50% of them have psychiatric illnesses. Meningeome actually is the most common tumor that presents with psychiatric symptoms in patients. So the way to think about how frontal lobe neoplasms cause pathology in the visual system is you can kind of separate it into non-localizing findings and localizing findings. We should all be familiar with the non-localizing findings which is your increased intracranial pressure symptoms so you know headaches which is positional trans-visual obscurations, diplopia, palcital tinnitus, but on findings of course we see papillodema associated with high ACP and unilateral bilateral six policies which are often called false localizing sign because they point to you in the wrong direction in terms of localization of pathology. And in terms of localizing findings, systemically they kind of relate to the areas of the frontal lobe that I mentioned to you which is the brokers which gives you expressive aphasia and prefrontal cortex which gives you the deficits in concentration and judgment and behavior and psychiatric symptoms and then of course the motor cortex which gives you contralateral paresis. In terms of the ocular findings which are relatively localizing would be something like foster Kennedy syndrome which we'll talk about in just a minute and the other thing that people do get in relationship to frontal eye field lesions is either deviation of the eyes towards the side of the lesion or they get acquired ocular motor apraxia. So I did want to spend a few moments talking about this because this is a really a favorite for exams and it is very clinically relevant. It happens pretty rarely I think probably in about one to two and a half percent of all the frontal lesions but this particular syndrome was described by Dr. Robert Foster Kennedy who was a neurologist in 1911 and he saw a patient who had a olfactory grovemen angioma and presented with this particular finding. So there are two main findings in Foster Kennedy syndrome. The first one is one optic nerve is atrophic and that is due to the compression of that optic nerve by the frontal tumor and the second finding is in the opposite eye there's optic nerve hetedema which is noted and that is related to the papillodema or to the increase intracranial pressure caused by the by the tumor. So as you can see in this image here from a recent case report it is the fact that this left eye has temporal pallor which is your finding number one and your left eye has this adematous optic nerve which is your finding number two. So this is Foster Kennedy syndrome. You cannot mention Foster Kennedy syndrome without mentioning pseudo Foster Kennedy syndrome which is a diagnosis of exclusion and the reason why it is a diagnosis of exclusion is you really should include real Foster Kennedy syndrome if you are going to claim somebody has pseudo Foster Kennedy syndrome and the most common etiology for that is sequential non-arturidic ischemic optic neuropathy. Other things that are in this differential are listed including arturidic ischemic optic neuropathy, optic neuritis among among others. On this image here you can see again that the left eye has some temporal temporal pallor and atrophy and on the right there is just the segmental optic nerve head swelling which is in keeping with a non-arturidic ischemic segmental optic neuropathy there. So I wanted to tell you about the outcome of this case which was somewhat unfortunate because you thought you might be saving somebody's life by sending them to the emergency room but she had a craniotomy and had her tumor removed. However a few kind of maybe a week or a week and a half later 10 days later she developed seizure like activity and some cognitive deficits and she had an intracranial hemorrhage with a right MTA stroke. She had to return to the operating room for a frontal lobectomy and a craniotomy again with clipping of pseudoradnurisms and had a kind of complicated hospital course and is just currently being transferred to the rehabilitation unit. Some of the most recent psychiatric and psychology notes say that she denies being depressed at this point but her frontal lobe is gone so she has some issues with mood and affect still which is consistently flat but when questioned she does not feel depressed. So just to review the three takeaway points first of all it's really important to think about the whole person as Laura mentioned and if you see somebody's past medical history listing depression or personality changes and ask more about it and in addition to that's unilateral optic atrophy we would recommend imaging those patients. You need to know what foster Kennedy's syndrome is and that is one-sided optic atrophy and contralateral discadema and the fact that the pseudo foster Kennedy's syndrome is generally due to non-artidic ischemic optic neuropathy among other causes lower in the differential. So I like to thank all the neuropathology team and I will take any questions. So and the other point that I would make is that I don't think your patient ever had documented optic nerve swelling in that eye and that's another reason to not make a diagnosis of ischemic optic. Do you know are there specific signs I mean among psychiatrists for instance that would kind of push that towards imaging patients. I imagine with that infrequent with being that infrequent it wouldn't. Yeah and in general I think if you look at you know other issues like metabolic abnormalities responsible for psychiatric illness it's it's not a huge percentage probably under 10% or so but they still routinely do things like thyroid testing etc. I think things to look for acutely you know I'm not psychiatrist I can't really claim but I think is is acute personality changes or acute changes in behavior those are always important if there's no risk factors associated with psychiatric illness those those are things to keep in mind as well. Great thank you.