Assorted Medications, Tests and Treatments




Mucor & Aspergillosis suspected:  amphotericin B

Invasive aspergillosis:  voriconazole


Category B  Animal reproduction studies have failed to demonstrate a risk to the fetus and there are no adequate and well-controlled studies in pregnant women.

Category C  Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks.

Category D  There is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience or studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks.



The doctors have reviewed with me the potential risks, side effects, alternatives, and complications of taking oral or intravenous steroids. We have also discussed the reasons for taking steroids, including the potential benefits, as well as alternative treatments in place of taking oral/intravenous steroids.

I understand that I should not use steroids if I have tuberculosis.

I understand the potential risks of taking oral/intravenous steroids include (but are not limited to) the following:

  • High blood sugar, which can trigger or worsen diabetes
  • Increased blood pressure, myocardial infarction, arrhythmias, cerebro-vascular disease
  • Increased risk of infections • Loss of calcium from bones, which can lead to osteoporosis and fractures
  • Gastro-intestinal ulcers, nausea, vomiting, stomach upset, liver problems
  • Weight gain, with fat deposits in your abdomen, face and the back of your neck eye pain
  • Avascular necrosis (cellular death of bone components due to interruption of blood supply) of hip bone/shoulder
  • Loss of calcium from bones with worsening of osteoporosis and fractures.
  • Elevated pressure in the eyes (glaucoma) • Cataracts; vision problems
  • Fluid retention, causing swelling in the eyes, face, hands, feet, legs
  • Skin acne, Thin skin, Easy bruising and Delayed wound healing
  • Mood swings (from mild irritability to severe mania, depression, seizures, suicidal ideation)
  • Insomnia
  • Suppressed adrenal gland hormone production
  • Menstrual irregularities in women

I understand and agree to the use of oral or intravenous steroid medication in the management of my condition. I also understand that I have other alternatives to the use of steroids.

With this knowledge of the potential risks, benefits, alternatives, and complications, I request that Dr. Ing proceed with the prescription of oral/intravenous steroids. I also acknowledge that Dr. Ing/his resident  ________________  have reviewed the use of this medication with me in detail, and answered all of my questions. I understand I should inform my family doctor/internist when I am starting steroids. I understand that should I experience a side effect I should contact my family doctor or head to the nearest emergency room.

Patient name:    ________________________________________________      Date:  _______________



Latent TB   (Test: quantiferon gold; Rx isoniazid/pyridoxine)

Hep B/C

Strongyloides stercoralis (Serology more practical than stool exam; Rx Ivermectin)

Pneumocystis jirovecii penumonia  (Rx Septra)



INFECTIONS:  HIV, Syphilis, VZV, HSV, Hepatitis, TB, Lyme

INFLAMMATIONS:  ANA, dsDNA, anti-ENA, RF, CRP, cANCA proteinase 3, ACE



Ach Receptor Ab.  (Mitogen)

Muscle-Specific Receptor Tyrosine Kinase (Musk) (Dynacare)

LRP4 Low Density Lipoprotein Receptor-Related Protein 4 Ab LDL Receptor-Related Protein 4 Ab   (London)






















Warnings and Precautions
Infusion Reactions: TEPEZZA may cause infusion reactions. Infusion reactions have been reported in approximately 4% of patients treated with TEPEZZA. Reported infusion reactions have usually been mild or moderate in severity. Signs and symptoms may include transient increases in blood pressure, feeling hot, tachycardia, dyspnea, headache, and muscular pain. Infusion reactions may occur during an infusion or within 1.5 hours after an infusion. In patients who experience an infusion reaction, consideration should be given to premedicating with an antihistamine, antipyretic, or corticosteroid and/or administering all subsequent infusions at a slower infusion rate.
Preexisting Inflammatory Bowel Disease: TEPEZZA may cause an exacerbation of preexisting inflammatory bowel disease (IBD). Monitor patients with IBD for flare of disease. If IBD exacerbation is suspected, consider discontinuation of TEPEZZA.
Hyperglycemia: Increased blood glucose or hyperglycemia may occur in patients treated with TEPEZZA. In clinical trials, 10% of patients (two-thirds of whom had preexisting diabetes or impaired glucose tolerance) experienced hyperglycemia. Hyperglycemic events should be managed with medications for glycemic control, if necessary. Monitor patients for elevated blood glucose and symptoms of hyperglycemia while on treatment with TEPEZZA. Patients with preexisting diabetes should be under appropriate glycemic control before receiving TEPEZZA.
The most common adverse reactions (incidence ≥5% and greater than placebo) are muscle spasm, nausea, alopecia, diarrhea, fatigue, hyperglycemia, hearing impairment, dysgeusia, headache, and dry skin.




Ozempic/Semaglutide 1mg sc weekly?

Glucagon-like peptide-1 (GLP-1) is a gut neuropeptide secreted by the distal small intestine in response to a meal.1 GLP-1 receptor agonists are existing therapeutic agents used in the treatment of diabetes. GLP-1 stimulates glucose-dependent insulin secretion and inhibits glucagon release, thereby lowering blood glucose but not causing hypoglycaemia.2 GLP-1 receptor agonists also signal at the hypothalamus to regulate satiety and weight.3 This has led to GLP-1 receptor agonists being licensed to promote weight loss in the setting of obesity

FL-41 LENS TINT  (Possible Sources Greater Toronto Area and Vancouver)

Credit Valley Optical: 2300 EGLINTON AVE W (Mississauga)

Eye Care Optical: 390 STEELES AVE W (Thornhill)

Spectrum Vision Care: 147 CLARENCE ST (Brampton)

Kanda Optical (Etobicoke)

Performance Vision Optometry  1242 Burrard St. (Vancouver)

Luxury Eyewear  415-650 41st Ave W (Vancouver)

“Are All FL-41 Migraine Relief Glasses Created Equal?” (

? order online and get shipped to Canada (?$15 shipping at Theraspecs). 

SCLERAL CONTACT LENS  a possible consideration for some patients with extreme dry eyes

Available from:

  • Steve Sanger, East York
  • Jennie Khalfan, Mississauga, Square One, Delta Optical
  • KEI Contact Lens Clinic
  • Vishakha Thakar, Vaughan
  • Jennifer Liao North York
  • Barbara Caffery, Shalu Pal downtown TO
  • Approximately $250 for fitting consultation and$500-1500 depending on which type of scleral fits best.




1. Online World Optic


2. Dr Bryanna Pinelli, Lunetterie,  482B Steele St, Port Colborne, ON L3K 6A7




? Abatacept, Ustekinumab, Anakinra
Strong consensus to use Idebenone as soon as possible at 900 mg/day (300 mg tid) in patients with disease less than 1 year.
e.g. Effinex™ Idebenone with Vitamin C 300mg
or    200 mg tablet + two 50 mg tablets = 300 mg

Not enough evidence to recommend treatment in chronic patients between 1 and 5 years (after the second eye onset), and no evidence to recommend treatment in chronic patients >5 years (after the second eye onset).

Carelli V, Carbonelli M, de Coo IF, et al.International Consensus Statement on the Clinical and Therapeutic Management of Leber Hereditary Optic Neuropathy. Journal of Neuro-Ophthalmology. 2017;37(4):371–381.  (idebenone–Raxone, Santhera Pharmaceuticals, Europe)




Mitogen website, St. Josephs Hospital

PARANEOPLASTIC:  CAR, MAR, CV2/CRMP5-antibody-related Paraneoplastic Optic Neuropathy


Neuromyelitis Optica Spectrum Disorder (NMOSD) and Myelin Oligodendrocyte Glycoprotein Antibody-associated Dis­ease (MOGAD)

NEUROMYELITIS OPTICA anti-aquaporin4 (AQP4) IgG antibody test for severe necrotizing ON.  NMO may have severe bilateral vision loss,  poor visual recovery, relapses, and may not show myelitis at onset.    ?plasmapheresis  (interferon, natalizumab and fingolimod may exacerbate disease course)

Drs. Chen and Moheb (Mayo Clinic) highlight:

  • NMOSD-ON is associated with poor visual outcomes. Therefore, early treatment with high-dose corticoste­roids and plasma exchange are recom­mended for acute attacks. All patients with NMOSD-ON require long-term treatment with an immunotherapeutic agent, such as rituximab or one of the recent FDA-approved monoclonal antibody treatments.
  • MOGAD-ON is usually responsive to high-dose corticosteroids and has a generally favorable visual outcome. However, some cases are corticosteroid dependent or have a relapsing disease course and require long-term main­tenance therapy; options include IV immunoglobulin or tocilizumab.
  • Because treatments for NMOSD-ON and MOGAD-ON are different from those for MS and other forms of ON, AQP4 and MOG antibodies should be checked in any patient with ON unless he or she has classic features of MS (both clinically and radiologically). The periventricular WM lesions typically seen in MS are rare in NMOSD-ON.
  • The FDA approved eculizumab, inebilizumab, and satralizumab for the treatment of NMOSD in 2019. Two clinical trials are enrolling patients with MOGAD in 2023 to investigate rozanolixizumab and satralizumab
NCI/NIH recommendation regarding immune related ADE with checkpoint inhibitors and other immunotherapy
If uveitis is anterior and mild to moderate (1-2+AC cell) and well controlled on topical therapy, the recommendations are to continue immunotherapy.
If more severe:  3+cell or more AU, IU, posterior or panuveitis the recommendations are to hold therapy potentially indefinitely depending on the clinical scenario.
Few other pearls on this topic:
1. ADE are seen more commonly in the following immune checkpoint inhibitors CTLA-4> PD-1>PD-L1
2. Uveitis is not a common ADE with immune checkpoint inhibitors (reported at 1%)
3. Most ocular immune ADE occur early (< 6 months)
4. Consider masquerades if later onset and no other systemic adverse related immune events (e.g.arthritis etc..)
5. Majority of reactions can be managed with topical or oral corticosteroids alone
6. Immune checkpoint related panuveitis that presents as a VKH phenotype may be seen more commonly in those who are being treated for cutaneous malignant melanoma


Dr. Daniel Yoshor:  Neurosurgeon at the University of Pennsylvania, NIH-funded cortical prosthesis research program

Dr. Nader Pouratian, Ronald Reagan UCLA, Orion visual cortical prosthesis (Second Sight)

Dr. Phil Troyk:  Scientist at Illinois Institute of Technology will enter Phase I trials with his visual cortical device

Dr. Patrick Degenaar’s talk on Neuroprosthesis (Newcastle University UK)



Dx: MRI with thin slices c and s contrast with fat sat sequences may show contrast-enhanced T1 enhancement of discrete segment of pre-chiasmatic optic nerve (time limited)

Rx: Intravenous bevacizumab:  The most commonly studied and used protocol for intravenous bevacizumab is a single dose of 5mg/kg q 2 weeks x 4   ?intravitreal bevacizumab

Other: Corticosteroids, hyperbaric oxygen, ?heparin, ?pentoxifylline

Most commonly used doses 5 mg/kg given every 2-3 weeks for 4-6 doses, but Zhuang 2019 has tried 1 mg/kg, once every three weeks, for at least three continuous treatments
5 mg/kg bevacizumab vs steroid for brain: Xu Y, Rong X, Hu W, et al. Bevacizumab Monotherapy Reduces Radiation-induced Brain Necrosis in Nasopharyngeal Carcinoma Patients: A Randomized Controlled Trial. Int J Radiat Oncol Biol Phys. 2018;101(5):1087‐1095. doi:10.1016/j.ijrobp.2018.04.068
Systematic review for brain: Delishaj D, Ursino S, Pasqualetti F, et al. Bevacizumab for the Treatment of Radiation-Induced Cerebral Necrosis: A Systematic Review of the Literature. J Clin Med Res. 2017;9(4):273‐280. doi:10.14740/jocmr2936e
Single arm study for patients refractory to steroids, anticoags, and HBO for brain: Furuse M, Nonoguchi N, Kuroiwa T, et al. A prospective, multicentre, single-arm clinical trial of bevacizumab for patients with surgically untreatable, symptomatic brain radiation necrosis†. Neurooncol Pract. 2016;3(4):272‐280. doi:10.1093/nop/npv064
double masked crossover study for brain: Levin VA, Bidaut L, Hou P, et al. Randomized double-blind placebo-controlled trial of bevacizumab therapy for radiation necrosis of the central nervous system [published correction appears in Int J Radiat Oncol Biol Phys. 2012 Sep 1;84(1):6. Grewal, Jai [added]]. Int J Radiat Oncol Biol Phys. 2011;79(5):1487‐1495. doi:10.1016/j.ijrobp.2009.12.061
Case series for radiation optic neuropathy: Dutta P, Dhandapani S, Kumar N, Gupta P, Ahuja C, Mukherjee KK. Bevacizumab for Radiation Induced Optic Neuritis Among Aggressive Residual/Recurrent Suprasellar Tumors: More Than a Mere Antineoplastic Effect. World Neurosurg. 2017;107:1044.e5‐1044.e10. doi:10.1016/j.wneu.2017.07.111
Additional case report for optic neuropathy: Farooq O, Lincoff NS, Saikali N, Prasad D, Miletich RS, Mechtler LL. Novel treatment for radiation optic neuropathy with intravenous bevacizumab. J Neuroophthalmol. 2012;32(4):321‐324. doi:10.1097/WNO.0b013e3182607381.



ALPHAEON® Beauty Eyelash Serum formulation  Peptide myristoly pentapeptide-17 which is in the, are thought to stimulate the keratin gene in the body; responsible for lash growth  (as opposed to the prostaglandin in Latisse)

LOTILANER  On June 2023, the US FDA approved XDEMVY (lotilaner ophthalmology solution 0.25%) for demodex blepharitis


ERIVEDGE (Vismodegib) from EyeWiki

Vismodegib (Erivedge) is a molecular inhibitor of the Hedgehog signaling pathway. It was developed by Genentech and approved by the FDA in January 2012 for the treatment of metastatic and locally advanced basal cell CA.

The hedgehog signaling cascade, which includes key receptor proteins such as Smoothened (SMO), have been implicated in cancers of the brain, lung, mammary gland, prostate and skin. The discovery of cyclopamine, an endogenous steroidal plant alkaloid that binds to SMO and inhibits downstream gene expression, initiated the quest for the identification of other agents that could inhibit the Hedgehog pathway.⁠ Vismodegib was one of the first such molecules to be developed and was originally used for the treatment of medulloblastoma.4⁠ It acts by binding to SMO and preventing the activation of downstream target genes.7⁠ When it was demonstrated in genetically engineered mice that the overactivation of the Hedgehog pathway was implicated in the development of other forms of cancer such as basal-cell carcinoma, investigators applied the Hedgehog inhibitors to halt these disease processes.

Vismodegib inhibits the Hedgehog signaling pathway. The Hedgehog pathway plays a crucial role during embryogenic development but has limited activity in most adult tissues, with the exception of hair, skin and stem cells.7, 9⁠ In more than 90% of BCC, the Hedgehog signaling pathway is abnormally upregulated.5, 10⁠ Mutations in key receptor proteins such as Patched (PTCH) and Smoothened (SMO) result in abnormal transcription of target genes that regulate basal cell growth and proliferation. Vismodegib acts as an SMO antagonist to prevent GLI1 and GLI2 transcription factor activation, blocking the signaling cascade.

Vismodegib is FDA approved ro the treatment of metastatic and locally advanced BCC that cannt be treated with surgery or radiation.  The dose of vismodegib is 150 mg orally once a day.

A Phase I clinical trial by Von Hoff et al. (2009)1⁠ studied the effect of vismodegib in three doses in 33 patients with metastatic or locally advanced basal-cell carcinoma: 150mg per day (17 patients), 270mg per day (15 patients) and 540mg per day (1 patient). Of the 33 patients, 18 had an objective response (2 complete, 16 partial), 11 had stable disease, and 4 had progressive disease. The median duration of response was 8.8 months. Molecular analysis of biopsy samples in 26 patients demonstrated over-expression of GLI1 mRNA expression in 25 patients. In a pharmacokinetic analysis, the median time to steady state was 14 days (range 7 to 22 days), and increasing the dose did not result in higher steady-state plasma levels. In 10 of 13 patients, there was a decrease in GLI1 expression by more than a factor of two in biopsy samples of treated patients compared with pretreatment biopsy-sample analysis. These findings confirmed the importance of the hedgehog pathway in basal-cell carcinoma and suggested the inhibitors of this pathway can be useful in treatment of these inoperable tumors.

A Phase II multicenter, international, two-cohort, nonrandomized study by Sekulic et al. (2012) studied the effect of vismodegib on patients with metastatic and locally advanced BCC.7⁠ Participants were deemed inappropriate surgical candidates based on multiple recurrences or substantial anticipated morbidity. All patients received once daily 150mg of oral vismodegib. In 33 patients with metastatic BCC, the response rate was 30% (95% confidence interval (CI), 16 to 48; P=0.001). In 63 patients with locally advanced BCC, the response rate was 43% (95% CI, 35 to 56; P<0.001) with complete responses in 13 patients (21%). The median duration for response was 7.6 months (range 1.0-12.9 months; 95% CI, 5.7-9.7).

A randomized, double-blind placebo-controlled trial by Tang et al. (2012) studied the effect of vismodegib on patients with the basal-cell nevus syndrome.11⁠ In 41 patients over a mean follow-up of 8 months, there was reduced per-patient rate of new surgically eligible BCC in the group treated with vismodegib than with placebo (2 vs. 29 cases per group per year, P<0.001). The size of existing BCC also showed significant reduction in the vismodegib group (-65% vs. -11%, P=0.003). The study also demonstrated a reduction of the hedgehog target gene expression by BCC by 90% (P<0.001) and diminished tumor-cell proliferation by analysis of the levels of messenger RNA encoding the hedgehog target gene glioma-associated oncogene homolog 1 (GLI1) in skin-shave biopsy samples of BCC taken at baseline and at 1 month after the start of vismodegib treatment.

Adverse Events:

In the Phase I clinical trial1⁠, there were 35 adverse events reported in total, of which 23 were grade 3 adverse events over a median follow-up time of 9.8 months. These included fatigue, hyponatremia, muscle spasm and atrial fibrillation. No dose-limiting toxic effects or grade 5 events were observed during the study period.

In the Phase II clinical trial7⁠⁠, adverse events occurred in more than 30% of patients with metastatic and locally advanced BCC, including muscle spasms, alopecia, dysgeusia (taste disturbance), weight loss and fatigue.

In Tang et al’s study11⁠, 54% of patients with basal-cell nevus syndrome (14 of 26) discontinued drug treatment due to adverse events. Patients receiving vismodegib were significantly more likely to experience adverse events compared to placebo, including hair loss, weight loss >5%, muscle cramps, and taste disturbance. Most adverse events were mild or moderate in severity, and no grade 5 events were observed.


Because of the importance of the Hedgehog pathway in embryogenesis and organ development, vismodegib is contraindicated in pregnancy. Vismodegib has been demonstrated to be teratogenic in rat studies and can result in craniofacial abnormalities, open perineum, retardation in normal growth, and absence or fusion of digits.8⁠ ⁠Patients of reproductive age should be counseled regarding the use of effective contraception while using this drug.

Other Hedgehog Inhibitors:

There have been other Hedgehog pathway inhibitors that have been developed for treatment of BCC besides Vismodegib. There are five other agents (BMS-833923 LDE224, LEQ506, IPI926 and TAK-441) that have shown promise in animal studies and early clinical trials.9⁠ For example, LDE225 is another selective antagonist of SMO protein. In a double-blind, randomized, vehicle-controlled study, twice daily topical treatment with 0.75% LDE25 cream in patients with the basal cell nevus syndrome resulted in partial responses in 9, complete responses in 3, and no clinical response in 1 out of 13 BCCs treated.12⁠


The use of Vismodegib is an example of selected, targeted molecular biology to treat aggressive basal cell carcinoma. The addition of this drug to the therapeutic armamentarium for recurrent, invasive or metastatic basal cell carcinoma is exciting. Anticipated are even more effective, selective drugs.


ALDARA  Imiquimod cream activates your body’s own immune system via a molecule called toll-like receptor 7 (TLR7), which in turn activates interferon-alpha to fight the cancerous cells.

Aldara Cream should be applied 5 times per week for a full 6 weeks to a biopsy-confirmed superficial basal cell carcinoma. An example of a 5 times per week application schedule is to apply Aldara Cream, once per day, Monday through Friday. Aldara Cream should be applied prior to normal sleeping hours and left on the skin for approximately 8 hours, after which time the cream should be removed by washing the area with mild soap and water.

IWash your hands before and after applying Aldara Cream. Wash the treatment area with mild soap and water before applying the cream, and allow the area to dry thoroughly.

Sufficient cream should be applied to cover the treatment area, including 1 centimeter of skin surrounding the tumor, but do NOT put Aldara near the eye. Aldara Cream should be rubbed into the treatment area until the cream is no longer visible.  Avoid contact with eyes, and lips.

Local skin reactions in the treatment area are common.  A rest period of several days may be taken if required by the patient’s discomfort or severity of the local skin reaction.

Early clinical clearance cannot be adequately assessed until resolution of local skin reactions (e.g. 12 weeks post-treatment). Local skin reactions or other findings (e.g. infection) may require that a patient be seen sooner than the post-treatment assessment for clinical clearance. If there is clinical evidence of persistent tumor at the post-treatment assessment for clinical clearance, a biopsy or other alternative intervention should be considered. Lesions that do not respond to therapy should be carefully re-evaluated and management reconsidered; the safety and efficacy of a repeat course of Aldara Cream treatment have not been established. If any suspicious lesion arises in the treatment area at any time after a determination of clinical clearance, the patient should seek a medical evaluation

Aldara Cream is packaged in single-use packets, with 12 packets supplied per box. Patients should be prescribed no more than 36 packets for the 6-week treatment period. Unused packets should be discarded. Partially-used packets should be discarded and not reused.



RITUXIMAB (see webpage above)


Each 1 mL of clear, greenish-yellow solution contains brimonidine tartrate 2 mg (0.2%).

Apo-Brimonidine P
Each 1 mL of ophthalmic solution, 0.15% .

Who should NOT take Apo-Brimonidine?

Anyone who is using monoamine oxidase inhibitors (phenelzine, tranylcypromine)


MYASTHENIA GRAVIS BLOOD TESTS:  LRP4, MUSK, Acetylcholine recpetor antibodies







? Methazolamide

Bendroflumethiazide (? 10 mg is very high dose)   Bendroflumethiazide is a very weak carbonic anhydrase inhibitor (does not affect urine ph as do acetazolamide and topiramate)

Analzye the stones.  Acetazolamide usually causes calcium phosphate or struvite stones.



2016 Revised AAO guideline

Excess is > 5 mg HCQ/kg actual body weight


VISUAL SNOW  dysfunctional sensory processing


Lamotrigine build slowly to  200 mg bid, and determine effect after a month on full dose

Acetazolamide 250 bid to maximum 1g.



The Canadian Ophthalmological Society does NOT support the medical use of cannabis
for the treatment of glaucoma due to the short duration of action, the incidence of
undesirable psychotropic and other systemic side effects and the absence of scientific
evidence showing a beneficial effect on the course of the disease. This is in contrast to
other more effective and less harmful medical, laser and surgical modalities for the
treatment of glaucoma.


VISUAL SNOW SYNDROME  Puledda, Francesca, et al. “Visual Snow Syndrome.” Neurology, vol. 94, no. 6, 2020, doi:10.1212/wnl.0000000000008909

A. Visual snow: dynamic, continuous, tiny dots in the entire visual field lasting >3 mo. • The dots are usually black/gray on white background and gray/white on black background; however, they can also be transparent, white flashing, or colored.

B. Presence of at least 2 additional visual symptoms of the 4 following categories: • (i)Palinopsia. At least 1 of the following: afterimages or trailing of moving objects. Afterimages should be different from retinal afterimages, which occur only when staring at a high-contrast Image and are in complementary color. • (ii) Enhanced entoptic phenomena. At least 1 of the following: excessive floaters in both eyes, excessive blue field entoptic phenomenon, self-light of the eye, or spontaneous photopsia. Entoptic phenomena arise from the structure of the visual system itself. The blue field entoptic phenomenon is described as uncountable little gray/ white/black dots or rings shooting over the visual field in both eyes when looking at homogeneous bright surfaces such as the blue sky; self-light of the eye is described as colored waves or clouds when closing the eyes in the dark; spontaneous photopsia is characterized by bright flashes of light. • (iii) Photophobia. • (iv) Nyctalopia.

C. Symptoms are not consistent with typical migraine visual aura.

D. Symptoms are not better explained by another disorder. • Normal ophthalmology tests (best corrected visual acuity, dilated fundus examination, visual field, and electroretinogram); not caused by previous intake of psychotropic drugs.