Medical Cases
with Janet

By: Rokaia Abdelhamid

Posted: 7/31/2026

Myasthenia Gravis

Marwa is a 23-year-old in dentistry school. She takes no medications and has no major health problems. She has no family history of any major disorder or disease.

For the past three weeks, she has been experiencing strong fatigue and muscle weakness. She reported that she exercises regularly but has been struggling due to fatigue. She said that by the end of the day after college, she noticed that her eyes were droopy, and her left eye was lower and more closed than her right. She also experienced double vision. She said that in the morning her eyes and sight are normal, but then throughout the day they get worse. She said these symptoms improve when she lies down and relaxes.

Marwa also reported that her daily activities, such as brushing her teeth and hair, showering, walking, and leaving things, became harder. She also said eating has become harder for her; she feels her jaw hurts, and she cannot swallow.

Symptomes

One eyelid is more droopy than the other

Muscle weakness

Fituge

Double eyesight

Jaw pain

Difficulty swallowing

Daily activities became harder

Symptoms get better when she relaxes

Physical Examination

During the physical examination, her strength and reflexes were initially normal. Marwa was asked to follow the physician's fingers without moving her head. After a minute, her eyelids started to droop. The physician asked her to raise both arms. After about a minute, she began to have difficulty keeping her arms up. She doesn't currently have any breathing problems.

Tests

The physician asked for some tests to be done:

Blood test: positive for acetylcholine receptor antibodies. Those attack the receptors that nerves use to signal muscles to move (Mayo Clinic, 2026).

Electromyography: It showed impaired electrical activity and communication between nerves and muscles (Mayo Clinic, 2026).

Repetitive nerve stimulation: The nerve that supplies that muscle receives little electrical pulses. These pulses measure the nerve's ability to communicate with the muscle. The nerve was tested

several times to determine whether it could send signals. The more it was tested, the worse it got because of fatigue. It showed that the nerves are tired, which may be a sign of myasthenia gravis (Mayo Clinic, 2026).

Chest CT Scan: shows enlarged thymus gland but no tumor.

Diagnosis

Marwa is diagnosed with generalized myasthenia gravis.

Myasthenia gravis is an autoimmune disorder. This means the immune system mistakenly attacks part of the body. In this condition, antibodies interfere with the signals that nerves send to muscles. As a result, the muscles become weak and tire more easily.

Treatment Plan

Pyridostigmine is one medication that enhances nerve-muscle communication. Although they are not a cure, these medications may help some people contract and strengthen their muscles (Mayo Clinic, 2026).

She could be prescribed immune-suppressing treatments, such as those that can reduce the production or activity of harmful antibodies.

Zilucoplan (Zilbrysq). This treatment consists of a daily injection that can be done at home. It helps prevent muscle injury by blocking a dangerous protein. Additionally, more recent treatments target a cell protein that accelerates the breakdown of dangerous antibodies. FcRN receptor blockers are the name of these more recent treatments (Mayo Clinic, 2026).

Life changes

- Take deeper breaths during the day

- Do difficult activities earlier when she has more energy

- Eat softer food, have small bites, and take her time while eating

Emergency plan

Marwa was told that if she started getting sharp pain, trouble breathing, and extreme fatigue, she should seek emergency help. The doctors can get an assessment at the moment and see if she needs surgery or an increase in her medication

Analysis

Marwa's symptoms point toward myasthenia gravis because her weakness changes throughout the day. She gets better after resting, but becomes weaker after repeatedly using the same muscles. The eyelid drooping and double vision suggest weakness in the eye muscles. Her jaw weakness and fatigue during workouts and daily activities, and her arm weakness after holding it up during the physical exam, suggest that the condition has spread beyond her eyes. A stroke is

less likely because her symptoms developed slowly and improved with rest. Also, no tumor was detected, and the rest of her tests support the final diagnosis.

Reflection

Before starting this assignment, I knew nothing about this disorder. While researching it, I learned a lot more, and it is actually quite interesting. Also, while writing this case study, I noticed that writing a case study is not as bad as I thought. It is like writing a story and requires your investigation to solve the riddle by connecting the dots and looking more closely at the details you have. It was a really nice experience, and I am glad we got to try this here.

Resources

Myasthenia gravis (MG). (2026, June 11). Cleveland Clinic.

https://my.clevelandclinic.org/health/diseases/17252-myasthenia-gravis-mg

Myasthenia gravis. (2026, June 5). Mayo Clinic.

https://www.mayoclinic.org/diseases-conditions/myasthenia-gravis/diagnosis-treatment/d rc-20352040

By: Vibha Gutta

Posted: 7/30/2026

Wilson Disease

A 22-year-old college student came to my clinic accompanied by his mother after experiencing progressive changes over the past year. His mother reported that he had always done well academically, but recently he had become forgetful, withdrawn, and increasingly irritable. He had begun struggling to complete assignments and had received complaints from his professors about his performance and his level of concentration. The patient also described episodes of fatigue and occasional abdominal discomfort but had dismissed it as stress. He denied alcohol or recreational drug use and he has no significant past medical history. There was no known family history of neurological disease, although he mentioned that one of his uncles died of liver disease in his thirties without a clear diagnosis.

During the examination, I noticed a mild tremor in both of the patient’s hands that became more noticeable when he attempted to write or reach for objects. His speech was slightly slurred, and his movements appeared slower than expected for someone his age. When asked to walk across the room, he demonstrated an unsteady gait with some loss of balance. He also had mild rigidity in his upper extremities and difficulty performing fast alternating hand movements. While maintaining eye contact, I noticed a faint brownish-green ring around the outer edge of both corneas. A neurological examination showed intact muscle strength but impaired coordination. Routine laboratory testing revealed elevated liver enzymes, but further blood work showed a low serum ceruloplasmin level with increased 24 hours urinary copper excretion. A slit-lamp eye examination confirmed the presence of Kayser-Fleischer rings.

Based on the patient’s neurological findings, abnormal liver function, low ceruloplasmin levels, elevated urinary copper, and the presence of Kayser-Fleischer rings, I diagnosed him with Wilson disease. Although his symptoms initially suggested several possible neurological conditions, including early-onset Parkinsonism or Huntington disease, the hepatic involvement and abnormal copper metabolism supported Wilson disease. To further confirm the diagnosis, I recommended genetic testing for mutations in the ATP7B gene. Since Wilson disease is an inherited disorder that causes excessive copper accumulation in the liver, brain, and other tissues, recognizing it early is important because the appropriate treatment can prevent permanent neurological damage and improve long-term outcomes.

The primary goal of treatment is to remove excess copper from the body while preventing further accumulation. I started the patient on trientine, a copper-chelating medication, because it increases urinary copper excretion and is generally well tolerated in patients with neurological symptoms. I also prescribed zinc acetate, which decreases intestinal copper absorption and serves as long-term maintenance therapy once copper levels are adequately controlled. I advised the patient to follow a low-copper diet by limiting foods such as shellfish, liver, nuts, chocolate, and mushrooms. Regular follow-up visits were scheduled to monitor liver functions, urinary copper levels, complete blood counts, and medication adherence. Because Wilson disease requires lifelong management, I also referred him to both a neurologist and a hepatologist to coordinate his ongoing care and monitor for disease progression.

This case shows how Wilson disease can initially present with subtle neurological and psychiatric symptoms that may easily be mistaken for more common disorders. The patient’s declining academic performance, personality changes, tremor, impaired coordination, and slurred speech pointed toward a neurological condition, while the abnormal liver enzymes showed that another organ system was also involved. The discovery of Kayser-Fleischer rings, with the laboratory evidence of impaired copper metabolism, helped narrow the diagnosis considerably. I selected trientine and zinc because the current treatment focuses on reducing the body’s copper burden and preventing future accumulation, which can slow or even reverse many symptoms when therapy begins early. This case shows the importance of considering rare but treatable disorders in young adults who present with unexplained neurological symptoms with liver abnormalities. Early diagnosis and consistent lifelong treatment offer the best opportunity to preserve neurological function and improve the quality of life.

References

Alkhouri, N., Gonzalez-Peralta, R. P., & Medici, V. (2023, May 15). Wilson disease: a summary of the updated AASLD Practice Guidance. PubMed. Retrieved July 17, 2026, from https://pubmed.ncbi.nlm.nih.gov/37184530/

EASL. (2025, March 13). New EASL-ERN Clinical Practice Guidelines on the management of Wilson’s disease. EASL-The Home of Hepatology. https://easl.eu/news/easl-cpgs-wilsons-disease/

Habash, N. (2024, May 13). In the Beginning: Neonatal Screening and Management of Wilson Disease. Liver Fellow Network. https://www.aasld.org/liver-fellow-network/core-series/clinical-pearls/beginning-neonatal-screening-and-management-wilson

By: Lydia Ghebrezghi

Posted: 7/29/2026

Glioblastoma

A 58-year-old man came into my office today with his wife, who seemed more concerned than he was. She explained that over the last three months, he had become increasingly forgetful and irritable. At first, they thought it was simply stress from work, but his symptoms gradually became more noticeable. He had difficulty remembering recent conversations, misplacing everyday objects, and occasionally struggling to find the right words while speaking. His wife also mentioned that he had recently begun making poor decisions at work and seemed less interested in hobbies he had enjoyed for years.

The patient reported experiencing frequent headaches that were worse in the morning and often later in the day. During the past two weeks, he had also experienced episodes of nausea and vomiting shortly after waking up. He denied having a history of migraines. He described feeling more tired than usual and admitted that he occasionally felt off balance while walking, especially when climbing stairs.

When talking with him, I noticed he frequently paused during conversaHons to search for words. During the neurological examination, he demonstrated mild weakness in his right arm and had difficulty performing rapid alternating hand movements on that side. His wife reported that about a week before the appointment, he briefly lost consciousness while eating dinner and experienced shaking movements lasting approximately one minute. He had never experienced a seizure before.

A neurological examination confirmed mild right-sided weakness and slowed cognitive processing. An MRI of the brain with contrast revealed a larger irregular ring-enhancing mass in the left frontal lobe with significant surrounding edema and a shift of the nearby brain structures. A biopsy was performed to determine the exact diagnosis.

Diagnosis

Based on the patient’s history, neurological examination, MRI findings, and biopsy results, I diagnosed him with glioblastoma, an aggressive Grade IV primary brain tumor. The location of the tumor in the left frontal lobe explains his personality changes, difficulty finding words, impaired judgment, right-sided weakness, and new-onset seizure. The headaches, nausea, and vomiting are consistent with increased intracranial pressure caused by the rapidly growing tumor.

Treatment Plan

Because glioblastoma grows quickly and infiltrates surrounding brain tissue, treatment should begin as soon as possible. I referred the patient to a neurosurgeon for maximal safe surgical removal of the tumor to reduce pressure on the brain and obtain as much tumor tissue as possible. Following surgery, I recommended combined radiation therapy and chemotherapy with temozolomide, which is considered the standard treatment for glioblastoma. I also prescribed dexamethasone to reduce swelling around the tumor and levetiracetam to help prevent additional seizures. Physical therapy and occupational therapy were recommended to improve strength and daily functioning after surgery, and I discussed palliative care resources and counseling to help the patient and his family cope with the diagnosis and maintain the best possible quality of life.

Analysis

This diagnosis was made because the patient’s symptoms developed progressively over several months and included headaches, personality changes, memory problems, language difficulty, right-sided weakness, and a new-onset seizure. Together with the MRI showing a ring enhancing brain mass and the biopsy confirming a Grade IV astrocytoma, these findings strongly support glioblastoma. While other neurological disorders such as stroke, brain abscess, or metastatic brain tumors can produce similar symptoms, the rapid progression, imaging findings, and pathology are most consistent with glioblastoma. Surgical resection followed by radiation and temozolomide chemotherapy remains the current standard of care because it can prolong survival, reduce symptoms, and improve quality of life, although there is unfortunately no cure for this aggressive cancer.

Works Cited

Adult central nervous system tumors treatment - NCI. (n.d.-a).

https://www.cancer.gov/types/brain/patient/adult-brain-treatment-pdq

Glioblastoma (GBM) - American Brain Tumor Association | learn more. (n.d.-d). https://www.abta.org/tumor_types/glioblastoma-gbm/

Glioblastoma - diagnosis and treatment - Mayo Clinic. (n.d.-b).

https://www.mayoclinic.org/diseases-conditions/glioblastoma/diagnosis-treatment/drc 20569078

Glioblastoma - symptoms and causes - Mayo Clinic. (n.d.-c).

https://www.mayoclinic.org/diseases-conditions/glioblastoma/symptoms-causes/syc 20569077

By: Julia Gatewood

Posted: 7/28/2026

Creutzfeldt-Jakob disease

Patient History & Symptoms

A 63 year-old woman came into my office today, alongside her daughter, 31. The patient seemed somewhat disoriented and confused, holding onto her daughter as she was led inside. Once the patient sat down, she began explaining that she had been having noticeable memory loss the past two weeks. She claimed that she had always had a relatively weak memory, however it seemed as if she was forgetting things at a more rapid rate as of recently.

The patient explained that she had been having trouble sleeping recently, and could not fall asleep for hours after going to bed. The patient also claimed that she would experience blurry vision and was struggling when it came to seeing different things. She said that she had never needed glasses prior.

The patient's daughter claimed that the patient was experiencing personality changes as well, sometimes getting very angry and other times very quiet and reserved. These changes were rapid, and never presented in the patient’s behavior prior. She also claimed that the patient was experiencing rapid, jerky movements and would even have trouble when it came to swallowing.

Throughout the visit, the patient struggled to remember certain things and would lose their train of thought when asked questions. The patient appeared to completely forget the topic of conversation and needed to have questions repeated multiple times. Sometimes she would have trouble speaking and articulating certain words.

When asked about previous medical history, she was having trouble recalling. Her daughter said that she rarely drank, never smoked, and did not do drugs. She had no previous medical conditions that related to her current symptoms. She did have a hearing aid that was administered to her 3 years ago. There was no family history of neurodegenerative disorders.

When asked to walk across the room to demonstrate mobility, the patient needed help from her daughter to get out of the chair. As she walked, she appeared wobbly and off-balance. Her behaviors were jerky and she was not coordinated.

Diagnosis & Treatment

Based on my observations, I suggested that an MRI be done to scan the brain for characteristic changes. I also suggested that a spinal fluid test (lumbar puncture) be done in order to rule out certain diseases. Upon these further tests, Creutzfeldt-Jakob disease was detected. Since there was no family history, it was likely to be developed sporadically. In cases of CJD, it is important to diagnose as soon as possible since the lifespan of patients with this disease is not long. CJD is very rare and only affects 1 in a million people. There is currently no treatment available for those who suffer with CJD. Because of this, I suggested to the patient's family to provide care in order to make the patient as comfortable as possible, and I got in contact with a specialist team. Certain psychological aspects of the patient’s condition, like anxiety or depression, could be helped with medication. On top of that, the muscle jerks and tremors could also be aided with prescription of medication as well. I advised the patient to draw up an advance directive for future treatment of their condition.

Analysis

Overall, I chose CJD because I had heard of prion disorders but did not know much about them. Although rare, it is important to be able to detect disorders like this and know how to continue with treatment. This case showcases the complexities of treating patients struggling with rare neurological disorders. The most important part is early recognition, as it is a very degenerative disease and must be detected early on. I made this treatment plan because I wanted to provide the patient with comfort and authority later on. Upon learning about advance directives, I wanted the patient to be able to choose options that worked for them, even if they were not able to communicate that later. I wanted to provide comfort to the patient when it came to the medications and prescriptions that could ease some of the symptoms of this disease (such as the mental costs, as well as the muscle spasms).

Citations

Mayo Clinic. (2023, January 28). Creutzfeldt-Jakob disease. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/creutzfeldt-jakob-disease/symptoms-causes/syc-20371226

Mayo Clinic. (2018). Creutzfeldt-Jakob disease - Diagnosis and treatment - Mayo Clinic. Mayoclinic.Org. https://www.mayoclinic.org/diseases-conditions/creutzfeldt-jakob-disease/diagnosis-treatment/drc-20371230

NHS. (2019). Treatment - Creutzfeldt-Jakob disease. NHS. https://www.nhs.uk/conditions/creutzfeldt-jakob-disease-cjd/treatment/

By: Deshna Khulbe

Posted: 7/27/2026

Dravet Syndrome

History

These parents came into my office today with their 10-month old baby boy, Richard. As soon as the family walked in, I noticed all of them looked very tired, and Richard appeared to be moody and cranky. Richard was trying to crawl and sit properly, but kept losing his balance and seemed hesitant to move around.

Parents reported that Richard had recovered from a high fever when he started having sudden, compulsive seizures about a week ago. During the episodes, Richard becomes unresponsive, his eyes deviate to the left, the left side of his body jerks rhythmically, followed by stiffening of his arms and legs. Afterwards, he is sleepy, irritable, and confused for nearly an hour. According to the parents, these seizures often last 7-10 minutes, often occurring in clusters, and happen about six times every day.

Even though the baby has recovered from the fever, his parents have noticed that the episodes still occur when he spends time outdoors in the warm weather. Richard also gets these seizures after taking hot-baths. Parents described that Richard would shake, twitch, and then stiffen after each episode. Parents also mentioned that Richard often has trouble sleeping since the seizure began.

After asking his parents for some background, they shared that Richard was born full-term after an uncomplicated birth and delivery. His parents mentioned that Richard had met his early milestones appropriately until the seizures began. At this time, Richard has been struggling to walk, and often loses his balance and control while crawling, grabbing and grasping.

Parents say there is no known family history of epilepsy, developmental disorders, or neurological conditions. Richard is not currently taking any medications other than acetaminophen (Tylenol) given during his recent fever.

Diagnosis

Based on the information Richard's parents gave, my physical examination, and the results of diagnostic testing, I diagnosed Richard with Dravet syndrome.

Because of the frequency and prolonged duration of Richard's seizures, he was admitted for further evaluation. Laboratory testing, including a complete blood count (CBC), electrolytes, glucose, and metabolic studies, was within normal limits, and an MRI of the brain showed no structural abnormalities. An EEG demonstrated epileptiform activity, and genetic testing later confirmed a pathogenic mutation in the SCN1A gene, supporting the diagnosis of Dravet syndrome.

Since there is currently no cure for Dravet syndrome, the primary goal of treatment was to reduce seizure frequency and improve Richard's quality of life. I prescribed him valproic acid and clobazam, two anti-seizure medications.I also discussed starting a ketogenic diet, a high-fat, low-carbohydrate diet.

Because fever and overheating are common seizure triggers in Dravet syndrome, I advised Richard's parents to avoid hot baths, monitor fevers closely, keep him well hydrated, and use fever-reducing medications when appropriate.

I also developed an emergency seizure action plan with Richard's family. If a seizure lasts longer than five minutes, they should administer intranasal midazolam as rescue medication and call emergency medical services immediately. During a seizure, they should place Richard on his side, protect him from injury, avoid placing anything in his mouth, and monitor his breathing until help arrives.

Analysis

Based on Richard's age, seizure history, and test results, Dravet syndrome was the most likely diagnosis. His seizures began before one year of age after a high fever, which is a significant trigger of Dravet syndrome. The seizures were prolonged, lasted five to seven minutes, occurred in clusters, and initially affected only one side of his body (hemiclonic seizures), all of which are characteristic of the disorder. In addition, his seizures continued even after the fever resolved and were triggered by hot baths, another common feature of Dravet syndrome. Richard also showed developmental regression, poor balance, delayed motor skills, and sleep disturbances, which are frequently seen as the condition progresses. Other possible causes, such as structural brain abnormalities, metabolic disorders, and infections, were ruled out through normal laboratory testing and MRI findings. Finally, the identification of a pathogenic SCN1A gene mutation confirmed the diagnosis of Dravet syndrome.

Sources

Cleveland Clinic. (2022, March 15). Dravet Syndrome: What It Is, Symptoms, Prognosis & Treatment. Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/22517-dravet-syndrome

Diagnosis and treatment - dravet syndrome foundation. (2022, April 3). https://dravetfoundation.org/hcp-resources/diagnosis-and-treatment/

National Institute of Neurological Disorders and Stroke. (2025, March 24). Dravet syndrome | national institute of Neurological disorders and stroke. Www.Ninds.Nih.Gov. https://www.ninds.nih.gov/health-information/disorders/dravet-syndrome

Strzelczyk, A., & Schubert-Bast, S. (2022). A practical guide to the treatment of Dravet syndrome with Anti-Seizure medication. CNS Drugs, 36(3), 217–237. https://doi.org/10.1007/s40263-022-00898-1

By: Adithi Pillai

Posted: 7/27/2026

Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS)

Patient History / Symptoms

A 10 year old male, Ethan, came into my office today with his mom. Immediately I noticed a constant “woohooing” sound (about every 2-4 minutes). I could not tell if it was voluntary or involuntary, but the mom hadn’t twitched at the noise suggesting it was a common practice. I also noticed a slight shoulder jerk sensation (every 3-4 minutes), again could not tell if the kid was simply fidgety or if it was involuntary.

Two weeks earlier, Ethan had a sore throat and a fever at 101.6 degrees Fahrenheit. She fed him chicken soup and tylenol, and the illness resolved after 4 days. Thus, she did not find a reason to visit the physician.

Then, that last Friday her son started complaining about how his favorite pajamas felt on his skin and was restless the entire night. Since Monday, she has also noticed the “woohooing” sounds and shoulder jerks. Additionally, Ethan is adamant about sleeping on the floor of his parent’s room. He is constantly getting up and checking the door to the parent’s room, trying to make sure it is closed all the way. His mom used the words: “This is not him.”.

There is no history of head trauma, new medications, big familial changes (divorce, loss), or psychiatric diagnoses.

Past history is as follows:

Full term birth, all developmental milestones met on time
3 confirmed episodes of streptococcal infection, confirmed with cultures adn trated with amoxicillin
No drug allergies
Has all vaccines
Mother’s sister has been diagnosed with OCD. Father’s brother and dad both have type 1 diabetes

As I went to examine him, I noticed a repetitive blinking pattern. Vitals were normal: 98.6 degree Fahrenheit temperature and 102/64 BP. His throat shows slight redness, but nothing abnormal. Regular heart rate and no murmur. The jerk movement, eye blinking, and sounds stayed constant throughout examination. Cranial nerves were intact, however. He was cooperative for the whole exam. He did ask about 10-12 times to see if the door was closed all the way.

Diagnosis

I ordered a rapid strep test (came back negative), throat culture (negative), ASO titer (elevated), Anti-DNase B titer (elevated), CBC with differential (normal), EEG (normal), and thyroid panel (normal).

The elevated ASO and Anti-DNase B reflect a recent Group A streptococcal infection. EEG shows no explanation for tic/movements. Thyroid panel reflects limited autoimmune/endocrine explanation.

I would diagnose Ethan with Pediatric Autoimmune Neurophysciatric Disorders Assciated with STreptococcla Infections (PANDAS). The diagnosis remains clinical, with no cofnrimatory laboratory test. Yet, Ethan satisfies each element.

OCD / tics: new door checking rituation, shoulder-shrug tics, and vocal tics
Prepubertal onset: age 10
Abrupt onset: happened in a single weekend
Secondary link to Group A Streptococcus infection: document sore throat and prior recurrent episodes (3-4 weeks before onset). Confirmatory elevated ASO and Anti-DNase B titers, even with now-negative cultures
Neurological abnormalities: motor tics, limited grip strength

Treatment

I have prescribed a course of amoxicillin. Although negative cultures, the body still is fighting GAS infection. Additionally, patients with PANDAS have had positive responses to amoxicillin.

The management of PANDAS is with claiming the immune system and managing any esutling symptoms. Thus, CBT was prescribed, specifically exposure and response prevention therapy to target OCD thoughts and behaviors.

I will follow up with this family in 5-7 days and refer them to pedantic neurology or rheumatology if symptoms and episodes persist. I will monitor for any new rounds of amoxicillin, additional behavioral therapies, or anxiety medications (if needed).

Analysis

The rapid onset of symptoms and the abnormal behavioral changes automatically pointed me into the neurological direction. However, as the mother continued to explain the history and ESPECIALLY the recurrent strep infections, I started linking the OCD as a result of Strep. The blood tests confirmed Group A Streptococcal infection (the one associated with PANDAS) and thus I came to the conclusion of PANDAS. It is important to treat any “elft-over” infection, even if cultures came back negative there are still excessive amounts of immune bodies. Additionally, since Ethan is so young I did not want to immediately prescribe psychiatric medication. If his symptoms can be managed with CBT and ERP that would be an easier shift for him.

Work Cited

Cleveland Clinic. (2022). Pandas syndrome: What it is, causes, symptoms & treatment. Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/23553-pandas-syndrome

Grandinetti, R., Mussi, N., Pilloni, S., Ramundo, G., Miniaci, A., Turco, E., Piccolo, B., Capra, M. E., Forestiero, R., Laudisio, S., Boscarino, G., Pedretti, L., Menoni, M., Pellino, G., Tagliani, S., Bergomi, A., Antodaro, F., Cantù, M. C., Bersini, M. T., … Esposito, S. (2024). Pediatric acute-onset neuropsychiatric syndrome and pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections: A delphi study and consensus document about definition, diagnostic criteria, treatment and follow-up [Review of Pediatric acute-onset neuropsychiatric syndrome and pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections: A delphi study and consensus document about definition, diagnostic criteria, treatment and follow-up]. Frontiers in Immunology, 15. https://doi.org/10.3389/fimmu.2024.1420663

Haridass, D. (2025). Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections: A comprehensive review [Review of Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections: A comprehensive review]. Rheumatology Advisor. https://www.rheumatologyadvisor.com/features/pandas-diagnosis-and-management-review/

National Institute of Mental Health. (2019). NIMH » PANDAS—Questions and answers. Www.Nimh.Nih.Gov. https://www.nimh.nih.gov/health/publications/pandas

Pandas | PPN. (2018). Pandas Physicians Network. https://www.pandasppn.org/pandas/

By: Nicea Ali

Posted: 7/26/2026

Aicardi Syndrome

Patient history and Symptoms

Today, 5-month-old Amaya was brought in by her parents after she had continuously experienced seizures. Her parents explained to me that Anaya is like a typical infant who spends most of her days in her family’s love and care.

However, at times, she occasionally had seizures in the past hour and experienced weakness in her muscles. Additionally, instead of rolling around, exploring objects, or even being curious about the world around her, her actions remained the same as her younger self. She has not really been rolling around like everyone else and responds a bit late after she is waved at. Along with that, her spine also seems to become a bit more rightward than her original structure. But besides these symptoms, there were no digestive problems as her consumption and excretion levels have remained normal. The blood pressure levels were also normal.

Her mom reported that the doctors had told her that there might be a small chance that there would be some complications with Anaya when she had an ultrasound. Her parents are most worried about her seizures and developmental delays and want Amaya to get the best treatment available after a proper diagnosis.

Diagnosis

After taking a look at her, I decided to order a few tests, which included an MRI, which would look for any abnormalities in the corpus callosum and other brain structures, an EEG, to confirm epilepsy, and an eye exam, to check for coloboma or choroidal lacunae.

Through these, I came to notice that a part of her corpus callosum was not fully formed. The purpose of this structure is to separate the left and right hemispheres of the brain. Additionally, the eye exam revealed that she has coloboma, which means that she is missing a tissue near the retina.

In this way, she is displaying the classic triad in which she is having seizures, has an incomplete corpus callosum, and has coloboma. Since her mom reported that a prenatal check-up already raised some concerns and she is a female, I am more certain of my diagnosis. As a result, I diagnosed her with Aicardi Syndrome.

Aicardi Syndrome is a very rare neurodevelopmental and epileptic disorder that occurs almost always in females. It can result in major changes and complications in the brain.

Treatment

Unfortunately, there is no cure for Aicardi Syndrome. However, there are ways to manage her symptoms. For seizure control, I will prescribe antiseizure medication such as Vigabatrin, which increases the inhibitory neurotransmitter GABA and stabilizes abnormal electrical activity to reduce seizures. Along with that, a vagus nerve simulator can also be implemented if medications are not successful in stopping the seizures.

Physical, occupational, and speech therapy can be utilized throughout her life to manage both her physical and developmental symptoms. Physical therapy will be beneficial for movement and mobility, as she is displaying signs of musculoskeletal issues. Occupational therapy can help her perform daily tasks, as she is showing signs of neurodevelopmental delays. Speech therapy can also help her improve her communication skills.

Furthermore, she has to have routine clinical visits to monitor growth, nutritional status, and safety of oral intake as she has to take medications long-term, seizure control, developmental progress and educational needs, respiratory function and aspiration risk, and the spine and degree of scoliosis.

In all, long-term management by a pediatric team with expertise in the management of infantile spasms and medically refractory epilepsy is essential.

Analysis

I came to the diagnosis of Aicardi Syndrome because Amaya showcases the classic triad, as found with the underdeveloped corpus callosum, the presence of coloboma, and recurring seizures. Not trying to roll around and slow response also confirms neurodevelopmental delays, as well as the prenatal ultrasound that highlighted abnormalities. While this is a very rare disorder, the confirmed signs and symptoms present a very clear identification of Aicardi Syndrome.

I chose this treatment plan because it is necessary for long-term care. Although there is no definitive cure, having regular visits to physical , occupational, and speech therapists will give her the best quality of life. Contacting special education programs in school will also ensure better management as well as support for her overall.

Works Cited:

Aicardi Syndrome: What It Is, Symptoms, Treatment & Prognosis

A Case of Aicardi Syndrome with Positive Outcomes Following Hemispherectomy (P10-9.015) | Neurology

Aicardi Syndrome - GeneReviews® - NCBI Bookshelf

Diagnostic approach to Aicardi syndrome: A case report - PMC

chorioretinal lacunae | Hereditary Ocular Diseases

By: Nailah Kusi

Posted: 7/24/2026

Tourette Syndrome

A 15-year-old male came into my office today with his mother because she was concerned about unusual movements and sounds that had gradually become more noticeable over the past two years. His mother explained that the symptoms first started as frequent blinking, which everyone assumed was caused by seasonal allergies. A few months later, he began shrugging his shoulders several times throughout the day. More recently, she noticed he had developed occasional throat-clearing sounds even when he was not sick.

The patient explained that before these movements happen, he feels a strange pressure or tingling sensation in his neck and shoulders that continues to build until he performs the movement. He said completing the movement provides temporary relief, but the feeling eventually returns. He also mentioned that he sometimes tries to suppress the movements during school because he does not want his classmates to notice. However, after school he experiences several movements in a short period of time because he has been holding them in all day.

His mother reported that his symptoms become worse when he is anxious, excited, tired, or under pressure at school. His teachers described him as an intelligent student but mentioned that he has become more distracted recently and occasionally has difficulty concentrating during class. They also noticed that other students sometimes stare or laugh when he makes unexpected noises, causing him to avoid participating in classroom discussions.

The patient denied any recent illness, head trauma, drug use, or alcohol use. He reported sleeping normally but admitted feeling embarrassed about his symptoms. His mother stated that one of his uncles experienced similar movements as a child that gradually became less severe during adulthood, although he was never formally diagnosed.

During the examination, I observed several episodes of rapid eye blinking, facial grimacing, shoulder shrugging, and occasional throat clearing. The patient remained alert and cooperative throughout the visit. His speech was clear, and his memory, attention, and thought process were appropriate for his age. Cranial nerves were intact, muscle strength was 5/5 in all extremities, sensation was normal, reflexes were normal and symmetric, coordination testing was normal, and his gait showed no abnormalities. No seizure activity or muscle weakness was observed during the examination.

Diagnosis

Based on the patient’s history, physical examination, and symptom pattern, I diagnosed him with Tourette syndrome. The patient has experienced multiple motor tics along with at least one vocal tic for more than one year, with symptoms beginning before the age of 18. His neurological examination was otherwise normal, making other neurological disorders less likely.

Treatment Plan

I discussed the diagnosis with both the patient and his mother and explained that Tourette syndrome is a neurological disorder rather than a behavioral problem. Since his symptoms were beginning to interfere with school and social interactions, I recommended Comprehensive Behavioral Intervention for Tics (CBIT), which teaches patients strategies to recognize and manage their tics. I also encouraged the family to meet with school staff to discuss classroom accommodations that could help reduce stress and embarrassment. If his symptoms continue to worsen or significantly interfere with his daily activities, medications such as guanfacine or aripiprazole could be considered after consultation with a pediatric neurologist. I also recommended regular follow-up visits to monitor his symptoms, emotional well-being, and overall quality of life.

Analysis

I chose Tourette syndrome because the patient’s history closely matches the diagnostic criteria. He has experienced both motor and vocal tics for more than one year, his symptoms began during childhood, and he describes the uncomfortable urge that occurs before the tic, which is commonly reported by patients with Tourette syndrome. His symptoms also become worse during periods of stress and improve after performing the movements, which further supports the diagnosis.

Other possible diagnoses were considered, including seizure disorders, medication-induced movement disorders, and other neurological conditions. However, these were less likely because the patient remained fully conscious during each episode, had a normal neurological examination, denied medication or drug use, and showed no evidence of muscle weakness, sensory loss, or abnormal coordination. Because his symptoms are currently affecting both his education and social life, behavioral therapy is an appropriate first-line treatment, while medication can be considered if his symptoms become more severe or difficult to manage.

Works Cited

Centers for Disease Control and Prevention. (2025). Diagnosis for Tourette syndrome. https://www.cdc.gov/tourette-syndrome/diagnosis/index.html

Mayo Clinic. (2025). Tourette syndrome: Symptoms and causes. https://www.mayoclinic.org/diseases-conditions/tourette-syndrome/symptoms-causes/syc-20350465

National Institute of Neurological Disorders and Stroke. (2025). Tourette syndrome. https://www.ninds.nih.gov/health-information/disorders/tourette-syndrome

By: Ryan Tran

Posted: 7/23/2026

Idiopathic Hypersomnia

Case

A 25-year-old man came into my office today and immediately I noticed he was slumped over in his seat with his back heavily arched. He explained to me that for the past 3-4 months every time he woke up, it would take him longer than usual to get out of bed. He said even walking to the bathroom was difficult at times and had trouble reaching for his toothbrush. As he was talking, his voice was very muffled and he was talking very slow. He also tells me that he falls asleep really early and averages 11-12 hours a night; he even said last week he slept for 14 hours and was extremely late for work.

I asked him about any potential stressors such as work or disruptions in his life. He told me that at work his co-workers have been needing to nudge him on the shoulder during meetings because he’ll occasionally lean into his chair and his eyelids will get heavy as if he’s ready for a nap. This happens even when he’s getting more than 11 hours of sleep. It can be hard to stay awake when sending emails, eating lunch, or driving home. He’s been trying over-the-counter caffeine pills because coffee has not been helping at all.

I next asked if he ever had suicidal or depressive thoughts which he was quick to shut down. He said he maintains a positive healthy life spending time with his wife and dog.

Based on his symptoms I sent him to see a neurosleep specialist to perform a polysomnogram and a multiple sleep latency test (MSLT) where his sleep was measured both during the night and through daytime naps. The results showed that despite having 10+ hours of sleep the night before, it took less than 8 minutes for him to fall asleep in each of the 5 measured naps. Additionally, his eye movement measured that he only fell into REM sleep once. Therefore, based on his reported symptoms and testing, this patient had Idiopathic Hypersomnia.

His paperwork reports that his sodium levels are normal and presents no risk for cardiovascular diseases, including no family history he says. I prescribed him with low-sodium oxybate which will allow his nighttime sleep to be more restorative and allow him to recharge at night without having to sleep for long. More restorative sleep at night will also reduce instances of daytime sleepiness. Finally, I also recommended that he stay off of medications that can alter his sleep.

This patient’s case shows how sleep disorders can bring disruptions to a person’s life and that it’s important to run specific tests to diagnose neurological sleep disorders. It’s also important to look at other factors like mental health and stress when it comes to irregularities in sleep. Idiopathic Hypersomnia can take hours away from people’s lives as sleep takes up half a day while they still experience intense drowsiness throughout the day. The condition’s cause is unknown and develops over time so it’s important to catch it as soon as possible before any significant harm is done.

Work Cited

Clinic, C. (2024, July 23). A multiple sleep latency test (MSLT) helps diagnose sleep disorders that cause daytime sleepiness. It happens after a sleep study. Cleveland Clinic. https://my.clevelandclinic.org/health/diagnostics/multiple-sleep-latency-test-mslt

Idiopathic hypersomnia - Symptoms and causes. (2017). Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/hypersomnia/symptoms-causes/syc-20362332

Wilson, S. (2026, May 8). Hypersomnia. Barrow Neurological Institute. https://www.barrowneuro.org/condition/hypersomnia/#overview

By: Samiha Saifudeen

Posted: 7/22/2026

Primary Lateral Sclerosis

Patient History

A 56 year old man came into my office today with his wife. As he walked into the room, I noticed that his movements were slow and stiff. He relied on a cane and seemed to drag both feet slightly with each step. When he sat down, he took longer than expected to get comfortable and had difficulty crossing his legs.

The patient explained that over the past three years he had gradually noticed stiffness in both legs that seemed to be getting worse. At first, he thought it was just aging or arthritis, but the stiffness continued to progress despite physical therapy. He now struggles to climb stairs, stand up from low chairs, and walk long distances without losing his balance. He denied numbness, tingling, or muscle pain.

His wife mentioned that over the last several months his speech had become slower and more strained, almost as if he had to work harder to pronounce words. Occasionally, he laughed or cried more easily than he used to, even when the situation did not seem to match his emotions. The patient denied any memory problems or changes in sensation. There was no family history of neurological disease.

During the neurological exam, I found increased muscle tone in both legs, exaggerated reflexes, and a positive Babinski sign. Muscle strength was only slightly reduced, and there was no significant muscle wasting or muscle twitching. MRI scans of the brain and spinal cord were unremarkable, and electromyography showed no evidence of lower motor neuron involvement.

Diagnosis

Based on the patient's history, physical examination, and test results, I diagnosed him with Primary Lateral Sclerosis (PLS).

Treatment Plan

Since there is currently no cure for PLS, treatment focuses on managing symptoms and maintaining quality of life. I prescribed baclofen to help reduce muscle stiffness and spasticity. I also referred him to physical therapy to improve flexibility, strength, and balance, as well as occupational therapy to help him continue performing daily activities safely.

Because his speech had become more difficult to understand, I recommended speech therapy to improve communication and monitor swallowing problems if they develop. I also discussed the importance of using assistive devices, such as a walker if needed in the future, to reduce the risk of falls. Regular follow-up appointments with a neurologist were scheduled to monitor disease progression and adjust treatment as necessary.

Analysis

I diagnosed Primary Lateral Sclerosis because the patient's symptoms developed slowly over several years and mainly involved upper motor neuron signs, including muscle stiffness, exaggerated reflexes, spasticity, and a positive Babinski sign. The absence of muscle wasting, fasciculations, and lower motor neuron findings on EMG helped distinguish PLS from amyotrophic lateral sclerosis (ALS). Other conditions such as multiple sclerosis, spinal cord disorders, and Parkinson's disease were considered but were less likely because of the normal MRI findings and the patient's pattern of symptoms. Since there is no cure for PLS, the treatment plan focuses on reducing muscle stiffness, improving mobility, preventing falls, and preserving independence for as long as possible.

Works Cited

Mayo Clinic. Primary Lateral Sclerosis (PLS). https://www.mayoclinic.org/diseases-conditions/primary-lateral-sclerosis/symptoms-causes/syc-20353968

National Institute of Neurological Disorders and Stroke. Primary Lateral Sclerosis Information Page. https://www.ninds.nih.gov/health-information/disorders/primary-lateral-sclerosis

Cleveland Clinic. Primary Lateral Sclerosis (PLS). https://my.clevelandclinic.org/health/diseases/17986-primary-lateral-sclerosis

By: Janet Li

Posted: 7/21/2026

Bell's Palsy

Case

The patient is a 53-year-old woman who came into the office today with her daughter. The patient walked in with her hand covering her right ear, and I immediately noticed significant drooping of the right side of her face, especially around the mouth area. The patient’s right eye appeared red and irritated. Her gait appeared normal.

The patient spoke softly and explained that she first felt difficulty moving the right side of her face starting yesterday morning, and since then, the right side of her face became more numb and she has had trouble blinking. The patient’s daughter added that she noticed her mother’s smile became uneven starting last night.

While speaking, the patient frequently used tissues to wipe her mouth. The patient explained that she has had increased drooling and also noticed difficulty spitting after brushing her teeth this morning. The patient’s speech was unclear at times, such as by mixing up “b” and “p” sounds.

The patient continued covering her right ear with her hand throughout this interaction. When asked about it, the patient stated that she feels pain in her right ear and sounds feel “too loud”. The patient describes the pain as dull and constant and noticed that it began 2 days ago.

When asked about her past medical history, the patient stated that they have Herpes Simplex Virus (HSV) and a history of hypertension. However, the patient states they do not think they had an active HSV outbreak recently.

During the neurologic exam, when asked to smile, only the left side of the patient's face moved while the right side did not move at all. When asked to raise her eyebrows, only the left eyebrow moved and the left side of the forehead wrinkled while the right side didn’t move.

The patient’s vital signs were within normal limits. CT results were normal.

Diagnosis

Based on the patient’s symptoms and exam results, I diagnosed this patient with Bell’s palsy.

Treatment

For the treatment plan, I first started the patient on ibuprofen to manage her ear pain. I also prescribed prednisone, a corticosteroid, to reduce inflammation and swelling of her facial nerve. As a result, this can support a faster and more complete recovery. I prescribed eye drops to keep the patient’s eyes moisturized while she regains the ability to blink and close her right eye. I also scheduled a follow-up appointment in 2 weeks to monitor the patient’s recovery progress. Symptoms of Bell’s palsy usually improve within 3 weeks and are fully resolved within 3 months in most individuals. However, I wanted to monitor progress, especially in the case that symptoms do not improve.

Analysis

I diagnosed the patient with Bell’s palsy, because many of the complications observed and described by the patient are common symptoms of Bell’s palsy. Specifically, the one-sided facial paralysis that extends to the forehead, pain in the ear on the affected side, and inability to control spit and blinking. In addition, the patient has a history of HSV, which is strongly linked to Bell’s palsy. This is because HSV can cause facial inflammation, which has been thought to lead to nerve damage and paralysis in Bell’s palsy. However, more testing and research is necessary to determine if this was the cause of this patient’s Bell’s palsy.

I ruled out the likelihood of stroke, because the patient’s CT results were normal, the patient was unable to move their forehead during the neurological exam, and the patient didn’t have one-sided paralysis in the rest of their body excluding the face.

Works cited

Mayo Clinic. (2024, March 15). Bell’s palsy. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/bells-palsy/symptoms-causes/syc-20370028

UNC School of Medicine. (n.d.). Bell’s palsy. Retrieved July 16, 2026, from https://www.med.unc.edu/ent/facialnervecenter/conditions/bells-palsy/

Cleveland Clinic. (2023, August 14). Bell’s palsy: What it is, causes, symptoms & treatment. Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/5457-bells-palsy

By: Gloria Zhang

Posted: 7/20/2026

Guillain-Barré Syndrome

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Patient History and Symptoms

A 34-year-old man came into my office today accompanied by his wife. As he walked into the examination room, I saw that he was moving very slowly and relied heavily on the wall for support. He explained that about two weeks ago he had recovered from what he thought was a "stomach bug" that caused diarrhea and abdominal cramps for several days. He had returned to work feeling fine until three days ago, when he noticed some tingling in both of his feet. At first, he assumed he had simply slept in an awkward position. Over the next several days, the tingling gradually spread upward into his calves. He also began feeling unusually weak when climbing stairs and had difficulty standing up from a chair without using his arms. Yesterday morning, he stumbled several times while walking and needed assistance getting into his car. His wife mentioned that he had dropped a coffee mug earlier that morning because his hands suddenly felt weak. The patient denied that he had any recent injuries, back pain, headaches, or changes in vision. He also has no history of diabetes, stroke, or neurological disease. He also takes no daily medications and states that he has no family history of muscle disorders. During the physical examination, I noticed that the patient struggled to rise from the exam table. His muscle strength was reduced in both legs and mildly decreased in both arms. Sensation to light touch was mostly intact except for persistent tingling in his hands and feet. When I tested his reflexes at the knees and ankles, they were absent on both sides. His cranial nerve examination was normal, although he told me that swallowing water had felt slightly strange earlier that morning. His breathing appeared normal, but he became mildly short of breath after walking a short distance down the hallway.

I ordered blood work, MRI imaging of the spine to rule out structural causes, nerve conduction studies, electromyography (EMG), and a lumbar puncture. Blood tests and MRI findings were unremarkable. However, the nerve conduction studies showed slowed nerve conduction consistent with a demyelinating peripheral neuropathy. Cerebrospinal fluid analysis demonstrated elevated protein levels with a normal white blood cell count.

Diagnosis

Based on the patient's rapidly progressive, symmetrical ascending weakness, loss of deep tendon reflexes, recent gastrointestinal illness, abnormal nerve conduction studies, and cerebrospinal fluid findings showing elevated protein with a normal cell count (albuminocytologic dissociation), I diagnosed him with Guillain-Barré Syndrome (GBS).

Treatment

Because Guillain-Barré Syndrome can progress quickly and may affect the muscles responsible for breathing, I admitted the patient to the hospital for close neurological and respiratory monitoring. His vital capacity and respiratory function would be checked regularly to determine whether ventilatory support might become necessary. I recommended treatment with intravenous immunoglobulin (IVIG) over five days to help reduce the autoimmune attack on his peripheral nerves and it is the go-to treatment for Guillain-Barre syndrome. Plasma exchange would be considered as an alternative if IVIG was not effective or did not work for the patient. The patient was also started on physical and occupational therapy early to maintain joint mobility, prevent muscle contractures, and improve strength during recovery. Pain management and prevention of complications such as blood clots and pressure injuries were also included in his care plan. I explained that while most patients recover over several months, recovery speed varies, and some individuals may experience lingering weakness or fatigue.

Analysis

This patient's symptoms was very suggestive of Guillain-Barré Syndrome because his weakness developed rapidly over several days, began in the lower extremities, and progressed upward in a symmetrical pattern. The history of a recent infection was an important clue, as GBS commonly develops after infections. The absence of deep tendon reflexes further supported a peripheral nerve disorder rather than a problem involving the brain or spinal cord. MRI findings ruled out spinal cord compression, while the ordered labs and analyses confirmed that the findings are characteristic of Guillain-Barré Syndrome. Immediate hospitalization and treatment with IVIG were appropriate because early intervention can shorten recovery time and reduce complications, particularly respiratory failure, which is one of the most serious risks associated with this condition.

Works Cited

Dimachkie, M. M., & Barohn, R. J. (2013). Guillain-Barré syndrome and variants. Neurologic Clinics, 31(2), 491-510. https://doi.org/10.1016/j.ncl.2013.01.005

Leonhard, S. E., Mandarakas, M. R., Gondim, F. A. A., Bateman, K., Ferreira, M. L. B., Cornblath, D. R., van Doorn, P. A., Dourado, M. E., Hughes, R. A. C., Islam, B., Kusunoki, S., Li, C.-Y., Meulstee, J., Rajabally, Y. A., Shahrizaila, N., Uncini, A., van den Berg, B., Walgaard, C., Willison, H. J., & Jacobs, B. C. (2019). Diagnosis and management of Guillain-Barré syndrome in ten steps. Nature Reviews Neurology, 15(11), 671-683. https://doi.org/10.1038/s41582-019-0250-9

National Institute of Neurological Disorders and Stroke. (2024). Guillain-Barré syndrome. https://www.ninds.nih.gov/health-information/disorders/guillain-barre-syndrome

Mayo Clinic. (2025). Guillain-Barré syndrome: Symptoms and causes.
https://www.mayoclinic.org/diseases-conditions/guillain-barre-syndrome/symptoms-caus es/syc-20362793

By: Srinika Kallem

Posted: 7/18/2026

Lewy Body Dementia

Case

A 72-year-old man came into my office today with his wife, who was concerned about several changes she had noticed over the past year. She explained that her husband had become increasingly forgetful, but unlike some memory disorders, his confusion seemed to come and go. Some mornings he was able to hold long conversations and remember recent events without difficulty, while other days he struggled to recognize familiar places or follow simple instructions.

The patient's wife also reported that he had recently begun seeing things that were not there. He frequently described seeing children playing in the living room or small animals running across the floor. Although he understood that these visions seemed strange, they felt very real to him. He denied hearing voices or experiencing paranoia.

The patient stated that he had been having trouble sleeping because he often acted out his dreams. His wife described several occasions where he yelled, punched, or kicked during sleep as if he were fighting someone. One night he accidentally struck her while asleep but had no memory of doing so when he woke up.

Over the past several months, he also noticed increasing stiffness in his arms and legs and felt that his movements had become slower. His wife mentioned that his posture had become more stooped, and he shuffled when he walked. He had fallen twice within the last three months after losing his balance while turning.

During today's examination, I observed that the patient appeared alert at first and answered questions appropriately. However, midway through the appointment, he became noticeably confused and had difficulty following the conversation before becoming more attentive again a short time later. His facial expressions were reduced, his movements were slow, and I noted mild rigidity in both upper extremities. His reflexes and sensation were otherwise normal.

A Mini-Mental State Examination showed mild cognitive impairment that varied throughout the visit. A brain MRI ruled out stroke, brain tumor, and normal pressure hydrocephalus. Blood tests, including vitamin B12 levels and thyroid function tests, were within normal limits. Because of the patient's fluctuating cognition, recurrent visual hallucinations, REM sleep behavior disorder, and Parkinson-like motor symptoms, further neurological evaluation supported the diagnosis.

Diagnosis

Based on the patient's history, physical examination, and diagnostic findings, I diagnosed him with Lewy Body Dementia (LBD).

Treatment Plan

I explained to the patient and his wife that Lewy Body Dementia is a progressive neurodegenerative disorder that affects both thinking and movement. Although there is currently no cure, treatment focuses on managing symptoms and maintaining quality of life.

I prescribed rivastigmine, a cholinesterase inhibitor, to help improve cognitive function and reduce hallucinations. Because individuals with Lewy Body Dementia are extremely sensitive to many antipsychotic medications, I advised avoiding these drugs unless absolutely necessary and only under close supervision by a neurologist.

To address his stiffness and slowed movements, I referred him to physical therapy to improve balance, strength, and mobility while reducing his risk of falls. Occupational therapy was recommended to help him remain independent with daily activities, and I encouraged regular exercise as tolerated.

For his sleep disturbances, I discussed improving sleep habits and recommended melatonin before considering stronger medications. I also advised his wife to make the home safer by removing tripping hazards, installing grab bars, and ensuring adequate lighting throughout the house.

Follow-up appointments with a neurologist and neuropsychologist were arranged to monitor his symptoms and adjust treatment as the disease progresses.

Analysis

I diagnosed Lewy Body Dementia because the patient's symptoms matched several hallmark features of the disease. His fluctuating cognition, well-formed visual hallucinations, REM sleep behavior disorder, and Parkinson-like movement problems strongly suggested LBD rather than Alzheimer's disease or Parkinson's disease alone. The normal MRI and blood work helped rule out other possible causes of dementia and movement disorders.

I chose rivastigmine because cholinesterase inhibitors are considered first-line treatment for improving cognition and reducing hallucinations in many patients with LBD. Physical and occupational therapy were recommended to improve mobility and maintain independence. Because patients with Lewy Body Dementia can have severe reactions to antipsychotic medications, avoiding these medications unless absolutely necessary is an important part of treatment. Overall, this treatment plan focuses on symptom management, patient safety, and preserving quality of life for as long as possible.

Works Cited

Alzheimer’s Association . “Dementia with Lewy Bodies.” Alzheimer’s Disease and Dementia, 2022,
https://www.alz.org/alzheimers-dementia/what-is-dementia/types-of-dementia/dementia with-lewy-bodies. Accessed 16 July 2026.

Alzheimer’s.gov. “What Is Lewy Body Dementia? | National Institute on Aging.” Www.Nia.Nih.Gov, 1 Apr. 2024,
https://www.alzheimers.gov/alzheimers-dementias/lewy-body-dementia. Accessed 16 July 2026.

Mayo Clinic. “Lewy Body Dementia - Symptoms and Causes.” Mayo Clinic, Mayo Clinic, 8 June 2021,
https://www.mayoclinic.org/diseases-conditions/lewy-body-dementia/symptoms-causes/s yc-20352025. Accessed 16 July 2026.

NIH National Institute on Aging. “Lewy Body Dementia: Causes, Symptoms, and Diagnosis.” National Institute on Aging, 27 Jan. 2025,
https://www.nia.nih.gov/health/lewy-body-dementia/lewy-body-dementia-causes-sympto ms-and-diagnosis. Accessed 16 July 2026.

By: Avni Loya

Posted: 7/16/2026

Narcolepsy

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Case

A 17-year old female high-school student walked into my clinic today. Her medical history showed an Adderall prescription for ADHD when she was 15, but she was taken off of the medication a year later because treatment didn't yield results. When she walked in, she was noticeably upset, and was using crutches.

Her parents had called to schedule an appointment, and they were concerned because at a recent parent-teacher conference, several teachers mentioned that the patient was distracted during class and often fell asleep. Her parents said she was “lazier than she used to be” and they were concerned because her diet hadn't changed and she exercised everyday.

The patient is on her school's varsity cheerleading team and participated in this sport for the past seven years. At the latest cheer competition a week ago, her team had placed first place. After winning, the patient collapsed and twisted her ankle, and she explained she needed crutches due to the fall. The patient described the collapse as “an episode unlike any other”. She said that she never lost consciousness but felt extremely weak.

Later that week, the patient was taking an exam at school and experienced the same loss of muscle tone. She collapsed off of her chair and again felt very weak. While I was discussing her symptoms with her parents, I noticed she looked drowsy and distracted. She put her head down for approximately five minutes, but woke back up and apologized profusely. She looked embarrassed but was alert when she had rewoken. I asked her if these “sleep attacks” happened often, and she replied that they happen a few times a week. Afterward, the patient looked distressed. Her parents explained that they had hired a therapist for her because she was stressed out from exams.

I asked the patient how many hours she sleeps every night. She responded that she normally sleeps approximately 8-9 hours, but still has extreme daytime sleepiness. I asked if she had ever sought treatment for EDS, and she said she's been to several pediatricians, psychiatrists, psychologists, and sleep specialists in the last year to try to get an accurate diagnosis for her condition, but her parents had concluded she was “just lazy”.

Overall, she was alert, present, and polite throughout our meeting. However, she did indicate signs of anxiety and stress like fidgeting with her hands and biting her nails. I believe her microsleep was an indicator of a sleep disorder.

Diagnosis

Her medical history showed idiopathic hypersomnia and depression which came back negative. Based her description of collapses which were likely caused by cataplexy, I suspected she has narcolepsy type 1. I ordered an overnight polysomnography followed by a multiple sleep latency test for her to rule out obstructive sleep apnea, and results confirmed my diagnosis

I scheduled another meeting with her to discuss the diagnosis and treatment plans. I explained that cataplexy attacks cause the loss of muscle tone, and often occur after extreme emotions. For her treatment plan, I decided on a mix of pharmaceutical and lifestyle changes.

For her EDS, I prescribed 200mg of oral Modafinil every morning. I also suggested she take daily naps, maintain a consistent sleep-wake schedule, and limit caffeine during the day. Lastly, I explained that having a therapist is excellent for anxiety, and it's important to limit stress because it can cause cataplexy attacks and EDS.

Reflection

This case highlights how difficult it can be to diagnose narcolepsy. It's often misdiagnosed as primary sleep disorders, anxiety disorders, epilepsy, or even schizophrenia, and many patients spend years searching for treatment before being correctly diagnosed. At first, her anxiety, collapses, tiredness, and history on Adderall can seem like depression or even “just laziness” when treatment doesn't work. In fact, a lot of narcolepsy treatments explain that their parents and teachers think they're lazy because of their daytime sleepiness. It shows the need for studies on narcolepsy and improving the diagnosis process.

Citations

“Diagnostic Criteria." Together in Motion for Better Sleep, Takeda Pharmaceuticals, Https://Tmtk.Com/Adult-Narcolepsy/Disease-Overview/Diagnostic-Criteria. Accessed 13 July 2026.

Disease Areas - Sleep Disorders | Alkermes, www.alkermes.com/disease-areas/sleep-disorders. Accessed 13 July 2026.

Modafinil (Oral Route) - Side Effects & Dosage - Mayo Clinic, www.mayoclinic.org/drugs-supplements/modafinil-oral-route/description/drg-20064870. Accessed 13 July 2026.

NarcolepsyLink Resources, www.narcolepsylink.com/resources/resource-center/. Accessed 13 July 2026.

Testing for Narcolepsy | Sleep Medicine, sleep.hms.harvard.edu/education-training/public-education/sleep-and-health-education-program/sleep-health-education-13. Accessed 13 July 2026.

Tips for Living with Narcolepsy | WAKIX® (Pitolisant), wakix.com/living-with-narcolepsy/tips-for-living-with-narcolepsy/. Accessed 13 July 2026.

By: Laksha Muruganandam

Posted: 7/15/2026

Multiple Sclerosis

A 30 year old woman came into my office today after being referred by her doctor because she had been having strange symptoms over the past several months. She explained that the symptoms would come and go. Sometimes she would feel fine for a few weeks, but then they would come back again.

The first symptom she noticed was blurry vision in her right eye. She said it hurt whenever she moved her eye, but after a few weeks her vision slowly went back to normal. About three months later, she started feeling tingling and numbness in her left arm and leg. At first she thought she had just slept in a weird position, but the feeling lasted for several days.

She also told me that she has been feeling much more tired than usual, even after getting a full night's sleep. She works as a third-grade teacher and said she has been having trouble making it through the school day because she feels so exhausted. She also noticed that walking long distances has become harder because her legs sometimes feel weak and heavy.

While talking to her, I noticed she walked a little slower than normal and seemed slightly off balance. During the physical exam, I found that her left leg was weaker than her right, and her reflexes were more active than expected. She also mentioned that her symptoms seem to get worse after taking hot showers or spending a lot of time outside in the heat.

She has no history of drug use or recent injuries, and there is no family history of neurological disorders.

Diagnosis

Based on her symptoms and the results of her tests, I diagnosed the patient with Multiple Sclerosis (MS).

An MRI showed several damaged areas on her brain and spinal cord where the protective covering around the nerves had been affected. A spinal tap also showed oligoclonal bands, which are commonly found in people with MS. Blood tests were normal and helped rule out other conditions that could cause similar symptoms.

Treatment Plan

Since there is no cure for multiple sclerosis, the goal of treatment is to help manage symptoms and slow the disease down.

I started the patient on a short course of high-dose steroids to help reduce inflammation during her current flare-up. I also referred her to a neurologist to discuss starting a disease-modifying medication, which can lower the number of future relapses and slow the progression of the disease.

I recommended physical therapy to help improve her strength and balance. We also talked about getting enough sleep, staying active without overdoing it, reducing stress, and avoiding getting overheated since heat makes her symptoms worse. She will also have regular follow-up appointments and MRI scans to keep track of how the disease is progressing.

Analysis

I diagnosed this patient with multiple sclerosis because many of her symptoms matched the disorder. Her blurry vision, numbness, muscle weakness, fatigue, and balance problems all pointed toward MS. Another clue was that her symptoms came and went instead of staying the same all the time, which is common in relapsing-remitting MS. The MRI and spinal tap confirmed the diagnosis.

I chose this treatment plan because steroids can help treat flare-ups, while disease-modifying medications can help prevent future attacks and slow the disease over time. Physical therapy and healthy lifestyle changes can also help the patient stay active and improve her quality of life.

References

Mayo Clinic. (2024). Multiple Sclerosis. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/multiple-sclerosis/symptoms-causes/syc-20350269

National Institute of Neurological Disorders and Stroke. (2025, January 31). Multiple Sclerosis. Www.Ninds.Nih.Gov. https://www.ninds.nih.gov/health-information/disorders/multiple-sclerosis

By: Shreya Sengupta

Posted: 7/13/2026

Amyotrophic Lateral Sclerosis

Patient History and Symptoms

A 58 year old male, Mr. Carter, came into my office today with his wife. As he walked into the room, I noticed that he had difficulty lifting his right foot and seemed to drag it slightly behind him. His wife explained that over the past eight months, he had become more clumsy and had fallen several times. She also said that he often dropped objects like his phone and coffee mug because his grip had become weaker.

When I spoke with Mr. Carter, I noticed that his speech was slightly slurred. He explained that he had been having trouble pronouncing certain words and that his tongue sometimes felt weak. He also mentioned that he had been experiencing muscle cramps in his arms and legs and occasional twitching in his shoulders. Even though he felt tired more often than usual, he denied having any numbness or loss of sensation

Mr. Carter stated that before these symptoms started, he was active and enjoyed hiking and working on home projects. However, he recently had to stop many of these activities because his muscles seemed to be getting weaker. He looked frustrated and worried because he was losing the ability to do things independently.

During the physical examination, I noticed that the muscles in his hands looked smaller than normal. His arms and legs were weak, and I could see small muscle twitches. His reflexes were stronger than expected. However, he didn’t have any numbness or problems with feeling things.

Diagnosis

Based on Mr. Carter’s symptoms and examination findings, I diagnosed him with Amyotrophic Lateral Sclerosis (ALS), which is also known as Lou Gehrig’s disease. To help confirm the diagnosis, I ordered an electromyography (EMG), which showed abnormal electrical activity in the multiple muscles. An MRI and blood tests were also performed to rule out other neurological disorders that can cause similar symptoms.

Treatment Plan

Unfortunately, there is currently no cure for ALS. However, there are treatments that can help slow the progression of the disease and improve quality of life. I prescribed riluzole, a medication that may slow nerve damage and slightly extend survival. I also discussed another medication called edaravone, which might help slow the decline in daily functioning for some patients.

I referred Mr. Carter to physical therapy to help maintain his mobility and reduce muscle stiffness. I also recommended speech therapy because of his increasing difficulty speaking. Since ALS can eventually affect breathing muscles, O explained the importance of regular respiratory evaluations and discusses future options like breathing support if it's needed. Additionally, I encouraged him and his family to seek counseling and support groups because coping with an illness like this can be emotionally difficult.

Analysis

I made this diagnosis because Mr. Carter showed many signs of ALS. He had progressive muscle weakness, muscle twitching, cramps, and muscle wasting without losing sensation. The combination of the upper motor neuron signs like increased reflexes, and lower motor neuron signs like the muscle atrophy, strongly suggest ALS. His symptoms also gradually worsened over several months, which is common in this disease.

I chose the treatment plan because even though ALS can’t be cured, early treatment can help manage symptoms and improve the patient’s quality of life. Medications like riluzole and edaravone might slow disease progression, while physical therapy, speech therapy and respiratory support can help patients be independent and comfortable as possible for a longer period of time.

Works Cited

Mayo Clinic. (2024, April 10). Amyotrophic Lateral Sclerosis (ALS). Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/amyotrophic-lateral-sclerosis/symptoms-causes/syc-20354022

Amyotrophic Lateral Sclerosis (ALS) - Diagnosis and Treatment - Mayo Clinic. (2024, April 10). Mayoclinic.Org; Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/amyotrophic-lateral-sclerosis/diagnosis-treatment/drc-20354027

Muscular Dystrophy Association. (2019, April 30). Amyotrophic Lateral Sclerosis (ALS) | Muscular Dystrophy Association. Muscular Dystrophy Association. https://www.mda.org/disease/amyotrophic-lateral-sclerosis

By: Jordane Donfack

Posted: 7/9/2026

Tolosa-Hunt Syndrome

The patient is a 30 year-old woman that has been receiving repeated check ups with me as her primary care physician due to her carnival incident that she suffered through around 10 weeks ago. Based on the trajectory of our visits that had been previously conducted, she seemed to have been healing fast, despite tremendous brain damage, particularly at the forefront of her temple. However, during our most recent visit I had noticed the right side of her under eye was protruding out and was slightly droopy (Amrutkar C et al, 2022).

This drew my attention because particularly as when patients come in with one side of their face exhibiting less muscle contraction that’s a clear indicator of a stroke. However, when asking her to raise her right hand and arm, everything seemed normal. In addition, her motor control was intact and there were no signs of aphasia when responding to the questions I was asking. She then proceeded to state that the symptoms had arisen a day or two after our previous appointment. She had fallen ill with a sinus Infection. Nothing serious to the point where she took no more than a couple tablets of Acetaminophen. However, the following day she woke up with a severe headache, located above her Sinuses. She exhibited limited eye movement, her lower eyelid was droopy, and her right eye was protruding out in an unnatural manner (Amrutkar C et al, 2022).

She was also experiencing mild symptoms, like fatigue and double vision. It came as a massive shock to her and me included because she had been recovering relatively well, despite having significant damage to her superior orbital fissure during her accident.

As a healthcare provider, I was glad she was not going through a stroke because that could pose more damage to her in the future. However, this information suggests that the damage to the superior orbital fissure, or the cavernous sinus has caused ipsilateral oculomotor nerve palsies, oculosympathetic paralysis, and sensory loss in the distribution of the ophthalmic (Kline LB, Hoyt WF, pg.2) Upon further questioning, she’s losing tremendous vision in her right eye contributing to the optic neuritis.

Further testing would have been conducted if there was more that could be done, but there’s no specific laboratory test despite checking for autoimmune disorders, such as lupus which we had already concluded had not caused these symptoms (Ahmed HS et al, 2024) So an MRI was ordered to show the inflammation of the cranial nerves to determine whether or not that was the cause of the symptoms she was experiencing. After getting the results back, it was confirmed that she was suffering through Tolosa-syndrome.

The syndrome has no cure, but can be treated with steroid doses recommended by the neurologist. Its causes are unknown, but it typically occurs after a series of trauma, inflammation, etc. Considering she had just been in a serious accident that damaged that portion of her brain it was clear that this was her diagnosis. She must now be carefully monitored by her ophthalmologist to ensure that she doesn’t lose her vision, any further. With doses of steroids recommended by her neurologist, some patients according to the studies say that it helps but 9 to 71% (Kline LB, Hoyt WF, pg.2) of patients but also they say that the symptoms can relapse. She requires continuous monitoring from here on out.

References

Kline LB, Hoyt WFThe Tolosa-Hunt syndrome Journal of Neurology, Neurosurgery & Psychiatry 2001;71:577-582.

Ahmed HS, Shivananda DB, Pulkurthi SR, Dias AF, Sahoo PP. Clinical profile and outcomes in Tolosa-Hunt Syndrome; a systematic review. J Clin Neurosci. 2024 Nov;129:110858. doi: 10.1016/j.jocn.2024.110858. Epub 2024 Oct 3. PMID: 39366127.

American Academy of Ophthalmology. Tolosa-Hunt Syndrome (https://eyewiki.aao.org/Tolosa-Hunt_Syndrome). Last reviewed: 12/24/2022. Accessed 9/5/2023.

Amrutkar C, Burton EV. Tolosa-Hunt Syndrome (https://www.ncbi.nlm.nih.gov/books/NBK459225/). 2022 Aug 8. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2023 Jan-. Accessed 9/5/2023.

By: Kritika Goel

Posted: 7/6/2026

Huntington's Disease

A 49 year old man, Mr. Anthony Gopal, came into my office today accompanied by his wife. As he sat down I saw that his leg bounced restlessly and his fingers tapped against his knee in small, jerky movements that didn’t seem fully under his control. I asked him to walk a short distance across the room, and noted that his gait had an unsteady, swaying quality, like he was under the influence but he denied any alcohol use.

His wife explained that over the past two years, she has noticed him becoming increasingly clumsy, often dropping dishes or knocking into furniture without realizing it. She said his personality has also shifted, describing him as more irritable and quick to snap at their children over small things, which she said is completely out of character for him. Mr. Gopal added that he has been struggling at work, where he used to handle complex spreadsheets with ease but now finds himself losing his train of thought partway through tasks and forgetting steps he has done a hundred times before.
His family history includes that Mr. Gopal’s father passed away in his early fifties after spending his last several years in a care facility, unable to walk or speak clearly, though the family was never given a clear diagnosis for what was happening to him. He described his father's hands and face as constantly twitching toward the end. He compared it to a puppet being pulled by invisible strings.

During the physical exam, I observed brief, irregular, like movements in his arms and shoulders that appeared and disappeared unpredictably, along with difficulty maintaining a steady gaze when I asked him to follow my finger with his eyes.

His wife mentioned that he has also started having trouble swallowing certain foods, occasionally coughing during meals. In regard to his mental state, Mr. Gopal admitted that he has had thoughts of just giving up entirely, since he feels like he is "losing pieces" of who he used to be and does not want his children to watch him decline the way he watched his father.

I ordered genetic testing along with an MRI of the brain to further evaluate his symptoms.

Diagnosis

Based on the combination of involuntary movements (chorea), the progressive cognitive decline affecting his executive function and memory, the marked personality changes including irritability and apathy, and a strong family history suggestive of an inherited pattern, I diagnosed Mr. Gopal with Huntington's Disease (HD).

Genetic testing confirmed an expanded CAG trinucleotide repeat in the HTT gene, consistent with this autosomal dominant disorder caused by a pathological amplification of CAG repeats within the HTT gene.
His MRI also showed early atrophy in the caudate nucleus, a finding commonly associated with this disease. His father's undiagnosed decline, including involuntary movements and progressive loss of function, also fits the pattern of an unrecognized case passed down through the family.

Treatment Plan

Since there is currently no cure for Huntington's Disease, I focused on a symptomatic and supportive treatment plan. To help manage Mr. Gopal’s uncontrollable movements, I prescribed a VMAT2 inhibitor, deutetrabenazine, which helps reduce involuntary movements associated with the disease.

Given his reports of irritability and the troubling comments about giving up, I referred him urgently to psychiatry for further evaluation and to begin treatment with an antidepressant, since HD is closely linked to depression, anxiety, and an increased risk of suicide. I also referred him to physical therapy to help improve his strength, flexibility, balance, and coordination, and to speech and swallowing therapy given his early difficulty with eating safely. Finally, I referred his family for genetic counseling, since his children may also carry the expanded gene and would benefit from understanding their own risk and options.

Analysis

I arrived at this diagnosis because Mr. Gopal’s case presented the classic triad seen in HD including motor dysfunction, cognitive decline, and psychiatric disturbances. His chorea, balance problems, and swallowing difficulty pointed toward a movement disorder, while his memory lapses and trouble completing familiar tasks suggested cognitive involvement rather than a muscular condition.

The personality changes and concerning comments about not wanting to watch himself decline"reflect the emotional toll that HD often takes, which is why I gave an urgent psychiatric referral. His father's undiagnosed but similar decline strongly supported a hereditary cause, which the genetic testing later confirmed. I chose deutetrabenazine specifically for the chorea since it is one of the standard pharmacologic options, and I built the rest of the plan around the understanding that HD requires a team approach involving neurology, psychiatry, physical therapy, and genetic counseling, since no single medication can address all of its effects. I made sure to offer plenty of resources since a diagnosis like this is heavy and already he described feeling mentally taxed.

Works Cited

Cleveland Clinic. (2026, May 6). Huntington's disease (HD): What it is, symptoms & treatment. Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/14369-huntingtons-disease\

UR Medicine. (n.d.). Conditions & treatments: Huntington's disease. University of Rochester Medical Center. https://www.urmc.rochester.edu/conditions-and-treatments/huntington-s-disease

Vega, A. J., Hernandez, G. V., O'Malley, P. A., Robin, C. J., Parra, A. N., Varrassi, G., Shekoohi, S., & Kaye, A. D. (2025, December 1). Overview of Huntington's disease and emerging treatment strategies: A narrative review. Cureus. https://doi.org/10.7759/cureus.98243

(Author not listed). Huntington's disease: Understanding its novel drugs and treatments. PubMed Central. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10664735/

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