United States

Authors: 
Muneeba Ali, MD, Lubaba Mukhtar, MD, Warda Naqvi, MD, Muhammad Ayub, MD. 

Background:
Today, we present the case of Mollaret’s meningitis in a 49-year-old male who was acutely distressed with a severe headache and associated back pain upon presentation to the emergency department. Remarkably, he experienced a complete resolution of symptoms within 24 hours of admission. This case provides an opportunity to highlight the clinical behavior of this rare condition, the critical role of detailed history-taking , the importance of maintaining a high index of suspicion in patients with a history of viral meningitis, and the eventual bold decision to discontinue all intravenous management in a patient exhibiting signs of meningitis, provided the symptomatology is consistent with a diagnosis of Mollaret’s meningitis.

Case Presentation:
A 49-year-old male with a past medical history of viral meningitis presented to the emergency department (ED) with the chief complaint of a gradually worsening headache, associated with lower back pain. A lumbar puncture was performed, revealing cerebrospinal fluid with 180/μL red blood cells, 228/μL white blood cells, a glucose level of 37 mg/dL, and a protein level of 152 mg/dL. His symptoms surprisingly resolved completely within 24 hours. HSV-2 was detectable on CSF DNA PCR, and his clinical course was highly consistent with Mollaret’s meningitis. All intravenous therapy was discontinued, and the patient was discharged home on oral valacyclovir 1 g every 8 hours to complete a 10-day course.

Discussion:
Mollarets Syndrome or benign recurrent aseptic meningitis collectively refers to two distinct medical conditions which are Mollaret’s meningitis and Mollaret&#39;s lymphocytic meningitis. Mollaret’s meningitis is characterized by recurrent episodes, which typically goes away within a week or so, whereas Mollaret&#39;s lymphocytic meningitis is a recurrent chronic inflammation of the meninges.

Symptoms of moderate syndrome typically include meningeal signs, as well as various neurological symptoms including confusion, altered consciousness, seizures, paresthesia and cranial nerve palsies. However, these symptoms vary between episodes and may not always be present. The most implicated causative organisms are varicella-zoster virus (VZV) and herpes simplex virus (HSV). Autoimmunity and genetic factors also play a role in pathogenesis.

The diagnosis of Mollaret’s syndrome often proves to be a challenge, as there are no specific diagnostic tests available for this rare neurological disorder. CSF analysis is usually a critical lab test to diagnose the syndrome and usually shows elevated levels of lymphocytes and protein in the CSF. Viral testing can identify the underlying causative agent.

Treatment of Mollaret’s syndrome usually includes managing the acute episode and preventing further attacks. The literature regarding the use of antiviral therapy in an acute episode or as longer term prophylaxis is currently mixed.

AMA Research Challenge 2025 

The Back Burn: A Case Report of Mollaret’s Meningitis in a Young Male.

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AMA Research Challenge 2024 

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Authors: 
Muneeba Ali, MD, Lubaba Mukhtar, MD, Warda Naqvi, MD, Muhammad Ayub, MD. 

Background:
Today, we present the case of Mollaret’s meningitis in a 49-year-old male who was acutely distressed with a severe headache and associated back pain upon presentation to the emergency department. Remarkably, he experienced a complete resolution of symptoms within 24 hours of admission. This case provides an opportunity to highlight the clinical behavior of this rare condition, the critical role of detailed history-taking , the importance of maintaining a high index of suspicion in patients with a history of viral meningitis, and the eventual bold decision to discontinue all intravenous management in a patient exhibiting signs of meningitis, provided the symptomatology is consistent with a diagnosis of Mollaret’s meningitis.

Case Presentation:
A 49-year-old male with a past medical history of viral meningitis presented to the emergency department (ED) with the chief complaint of a gradually worsening headache, associated with lower back pain. A lumbar puncture was performed, revealing cerebrospinal fluid with 180/μL red blood cells, 228/μL white blood cells, a glucose level of 37 mg/dL, and a protein level of 152 mg/dL. His symptoms surprisingly resolved completely within 24 hours. HSV-2 was detectable on CSF DNA PCR, and his clinical course was highly consistent with Mollaret’s meningitis. All intravenous therapy was discontinued, and the patient was discharged home on oral valacyclovir 1 g every 8 hours to complete a 10-day course.

Discussion:
Mollarets Syndrome or benign recurrent aseptic meningitis collectively refers to two distinct medical conditions which are Mollaret’s meningitis and Mollaret's lymphocytic meningitis. Mollaret’s meningitis is characterized by recurrent episodes, which typically goes away within a week or so, whereas Mollaret's lymphocytic meningitis is a recurrent chronic inflammation of the meninges.

Symptoms of moderate syndrome typically include meningeal signs, as well as various neurological symptoms including confusion, altered consciousness, seizures, paresthesia and cranial nerve palsies. However, these symptoms vary between episodes and may not always be present. The most implicated causative organisms are varicella-zoster virus (VZV) and herpes simplex virus (HSV). Autoimmunity and genetic factors also play a role in pathogenesis.

The diagnosis of Mollaret’s syndrome often proves to be a challenge, as there are no specific diagnostic tests available for this rare neurological disorder. CSF analysis is usually a critical lab test to diagnose the syndrome and usually shows elevated levels of lymphocytes and protein in the CSF. Viral testing can identify the underlying causative agent.

Treatment of Mollaret’s syndrome usually includes managing the acute episode and preventing further attacks. The literature regarding the use of antiviral therapy in an acute episode or as longer term prophylaxis is currently mixed.

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Background: Intracranial hypertension (IH) is a rare but serious complication of growth hormone (GH) therapy. Incidence is roughly 13 per 100,000 cases. Risk factors for GH-induced IH include obesity, chronic renal failure, and Turner Syndrome. Blindness and intractable headache are primary concerns. GH therapy discontinuation is commonly sufficient for resolution of IH, but some patients require additional therapies. Most cases resolve within 12 months of GH discontinuation with favorable outcomes. We describe an unusual case of a very prolonged course of IH after GH therapy.

Case Presentation: A 19-year-old non-obese female developed persistent intracranial hypertension at age eleven within two months of starting GH therapy (0.264 mg/kg/week) for GH deficiency. Initially, she presented with new-onset headaches, pulsatile tinnitus, visual obscurations, and bilateral grade 1 papilledema. Lumbar puncture (LP) revealed an opening pressure of 44 cm H2O, and neuroimaging revealed a congenital hypoplastic transverse sinus. Despite promptly discontinuing GH therapy, symptoms remained persistent eight years later (opening pressure: 29 cm H2O; elevated OCT RNFL measurements: OD 120 um, OS 121 um). Her course was resistant to multiple standard diuretics (acetazolamide, topiramate, furosemide) and she was treated with repeated LPs for symptom relief. Her headache phenotype evolved into chronic migraine (16 days/month, MIDAS=69, severe) with medication overuse headache.

Discussion: Through our literature review of 169 reported cases, we found that symptom onset of GH-induced IH was typically within three months. Growth hormone discontinuation alone was often sufficient for symptom resolution, but up to 43% of patients underwent additional treatments– most commonly with acetazolamide, but interventions also included serial LPs, and, rarely, ventriculoperitoneal shunts. The prognosis is favorable. In those with detailed data, an estimated 95% reported resolution by 6 months and 98% by 12 months. Two cases reported complete resolution at 2 years after discontinuation. At 8 years, our patient’s duration is unusually prolonged. Although CSF pressures have improved over time, this is the longest persistence of GH-induced IH to the best of our knowledge. IH is an uncommon event during GH treatment, but our patient's course demonstrates the potential for long-lasting and debilitating adverse effects. Routine ophthalmological monitoring and a high index of suspicion is essential for early recognition, enabling timely interventions to prevent vision loss and headache disability.

Eight-Year Persistence of Growth Hormone-Induced Chronic Migraine and Intracranial Hypertension

Abstract Title
A Clot Conundrum: Reassessing Interstitial Lung Disease as Pulmonary
Embolisms with Aubagio Use
Background
Interstitial lung disease and pulmonary embolism are rare side effects reported post
teriflunomide use. Based on a trial evaluating the potential long-term effects of teriflunomide, reports of such adverse reactions have emerged from the TOWER extension study1 as well as several case studies2,3,4 . There are case reports of suspected pneumonia with a CT angiogram performed upon lack of clinical improvement, with pulmonary embolisms found there after. Here we report a case of suspected interstitial lung disease in the setting of teriflunomide use and upon further investigation, multiple pulmonary embolisms were discovered.
Case Presentation
A 46 year old female with a past medical history of multiple sclerosis, who was started on Teriflunomide four years prior, presented with progressive dyspnea, with persistent deoxygenation for one year based on an Apple watch monitoring device. The patient had several CT chest without contrast studies that were suggestive of interstitial lung pneumonitis prompting discontinuation of Teriflunomide and initiation of steroids. When the patient had no clinical improvement, a CT Angiogram with contrast later revealed extensive pulmonary artery emboli at multiple levels. Transthoracic echocardiogram revealed significant right heart strain. She was then started on a heparin drip and underwent a bilateral pulmonary endarterectomy.
Following this, the patient was started on oral anticoagulation and was continued on steroids.
Discussion
There have been a few reported cases of either interstitial lung disease and pulmonary embolism linked to Aubagio use in multiple sclerosis patients. In our case, a patient presumed to have interstitial lung disease was later diagnosed with multiple pulmonary embolisms. A more comprehensive evaluation of potential side effects could have resulted in earlier, more effective treatment. Thus, we caution against solely attributing symptoms to one side effect and recommend early consideration of multifactorial and broader adverse effects of Aubagio.

A Clot Conundrum: Reassessing Interstitial Lung Disease as Pulmonary Embolism with Teriflunomide Use

Background
Gradenigo syndrome is an uncommon complication of otitis media, first described by Giuseppe Gradenigo in 1904. The infection spreads from the middle ear to the petrous apex of the temporal bone, irritating cranial nerves V and VI. It classically presents with a triad: otorrhea, abducens palsy, and facial pain in the V1/V2 distribution. Although less common today due to antibiotics, diagnosis and management remain challenging, particularly when caused by atypical etiologies such as neoplasms.
We present a rare case of Gradenigo syndrome secondary to a meningioma in a 78-year-old female, emphasizing the importance of considering neoplastic causes and utilizing neuroimaging in patients with progressive cranial neuropathies and a history of brain tumors.
Case Presentation
A 78-year-old female with a history of four meningiomas and immune thrombocytopenic purpura (ITP) presented with generalized weakness, 3-4 months of painless diplopia, and significant unintentional weight loss.
Neurologic exam revealed bilateral lateral gaze palsies, left proptosis, suspected CN III/IV/VI palsies on the left, right CN VI palsy, and mild left facial droop. She also had left-sided hemiplegia from a prior stroke. Rinne test was positive on the right, negative on the left; Weber test was normal.
Labs showed hemoglobin of 9.4, platelets 51,000 (rising to 78,000), and ESR of 120 mm/hr.
Head CT showed no acute findings. MRI revealed a 3.7 cm enhancing lesion at the left cavernous sinus involving the dura, prepontine cistern, and sella, consistent with a meningioma compressing the pons. Another lesion at the petrous temporal bone was compressing cranial nerves.
Neurosurgery was consulted, and outpatient follow-up was advised.

Discussion 
This case illustrates a rare instance of Gradenigo syndrome mimicking infectious petrositis but caused by a skull base meningioma. Persistence of symptoms despite antibiotics and absence of infection signs pointed to a structural lesion.
Although the full triad was not present, many cases are incomplete. Accurate diagnosis requires maintaining a broad differential and early neuroimaging. Without it, tumors may be mistaken for infection, delaying care.
Other mimics include skull base infections, thrombosis, coagulopathies, Lemierre’s syndrome, and neoplasms. While antibiotics are standard for infectious cases, mass lesions often require surgery, thus, early recognition of atypical causes is critical to prevent lasting deficits. Even benign meningiomas can present deceptively at the skull base, warranting timely imaging.


A Rare Presentation of Gradenigo Syndrome Secondary to Skull Base Meningiomas: A Case Report

Background:
Ulnar neuropathy is the second most common upper extremity entrapment neuropathy, typically occurring at the cubital tunnel or Guyon’s canal. Simultaneous compression at both sites, referred to as “double crush syndrome” is not common; examples of double entrapment involving compression and cubital tunnel entrapment unrelated to trauma are rare. Reports of dual-site entrapment in otherwise healthy athletes, particularly from overuse, are exceedingly uncommon. We present a novel case of unilateral, double-site ulnar neuropathy in a hypermobile gymnast following repetitive handstands; an activity not previously associated with this condition.
Case Presentation:
A 30-year-old left-handed professional gymnast presented with acute paresthesia, weakness, and pain in the fourth and fifth digits of her left hand following a performance involving prolonged handstands. She repeated the routine the next night, after which symptoms intensified. Neurological examination showed decreased grip strength, weakness in finger abduction, and reduced sensation in the ulnar distribution. Tinel’s sign was positive at both the cubital tunnel and Guyon’s canal. Froment’s sign and the elbow flexion test were also positive. The patient reported frequent long-duration handstands several times per week and demonstrated hypermobility at the wrists and elbows. Radiographs were unremarkable; electromyography and nerve conduction studies was deferred due to improvement. At one-month follow-up, after pausing performances but continuing to coach, her symptoms largely resolved, consistent with overuse-related ulnar neuropathy exacerbated by joint laxity and load-bearing mechanics.
Discussion:
Hypermobility increases joint laxity and amplifies tensile and compressive forces on the ulnar nerve. Anatomical variations may further predispose to entrapment; close to 60% of patients had anatomical changes in the cubital tunnel that caused the ulnar nerve neuropathy, of which nearly 20% of patients had a subluxation of the ulnar nerve.
Hypermobile athletes may have unrecognized variants that tolerate extreme ranges but place neural structures at risk. During handstands, prolonged elbow extension and wrist hyperextension stress the ulnar nerve at multiple points. At the elbow, compression may occur at the retrocondylar groove, beneath Osborne’s ligament, between the flexor carpi unaris heads, or due to variants like the Arcade of Struthers or anconeus epitrochlearis. At the wrist, Guyon’s canal and pisohamate arch can entrap the motor branch, while trauma to the nearby ulnar artery may produce secondary compression (Hypothenar Hammer Syndrome). Unilateral symptoms may reflect dominance or asymmetric loading. Recognizing handstands as a potential biomechanical risk factor may guide early intervention and inform preventive strategies in similar athletic populations.

A Balancing Act: Dual Ulnar Nerve Entrapment In AHypermobile Handstand Performer

Background: Chimeric Antigen Receptor T-cell (CAR-T) therapy has transformed treatment for hematologic malignancies but is associated with immune effector cell-associated neurotoxicity syndrome (ICANS), a complication typically marked by cortical dysfunction such as encephalopathy, aphasia, and seizures. Current ICANS grading criteria uses the Immune Effector Cell-Associated Encephalopathy (ICE) score and relevant neurologic findings, with motor deficits falling under grade 4. However, spinal cord–predominant presentations are rare and not well represented in existing grading criteria.

Case Presentation: A 30-year-old female with refractory B-cell acute lymphoblastic leukemia and KMT2A rearrangement underwent CAR-T therapy with brexucabtagene autoleucel. After developing cytokine release syndrome (CRS), she experienced a progressive decline in mental status consistent with grade 2 ICANS. Despite aggressive immunosuppression with corticosteroids, tocilizumab, and anakinra, she developed sudden paraplegia and bowel/bladder dysfunction by day 8 post-infusion. MRI revealed diffuse T2 hyperintensities and cord expansion throughout the cervical and thoracic spinal cord, consistent with inflammatory myelitis. Intrathecal cytarabine and hydrocortisone were administered, followed by intravenous immunoglobulin (IVIG). While her cognitive status fully recovered, motor deficits persisted and only some sensory function recovered. At one-year follow-up, she remained paraplegic with persistent spinal cord atrophy and T2 intensities demonstrated on MRI.

Discussion: Spinal cord-predominant ICANS is a distinct clinical presentation that challenges current pathophysiologic models centered on cortical dysfunction. The decoupling of cognitive recovery from persistent motor deficits suggests a localized spinal cord injury, likely mediated by cytokine-induced blood–spinal cord barrier disruption. Spinal MRI was key to diagnosis, and earlier imaging may have facilitated more targeted intervention. Current ICANS grading systems, which rely heavily on ICE scores and encephalopathy, may overlook spinal presentations, delaying diagnosis and treatment. Revised grading criteria that account for spinal cord involvement, as well as research into optimal management strategies, are warranted to better identify and treat this rare but serious form of neurotoxicity.

A unique case of spinal-predominant ICANS with long-term motor deficits after CAR-T therapy

Background:
Keratoconus is a progressive, non-inflammatory corneal ectasia that often escapes diagnosis until complications arise. Acute corneal hydrops, a rare vision-threatening complication, results from a rupture in Descemet’s membrane, leading to sudden stromal edema. Long-term outcomes can depend on effective patient education, especially in individuals experiencing communication challenges or developmental delays. Early identification, appropriate management, and patient education are essential in reducing morbidity and preventing recurrence or progression.

Case Presentation:
A previously healthy young adult with developmental delay presented with a 24-hour history of severe left eye pain, corneal cloudiness, photophobia, and sudden vision loss. Visual acuity tested at count-fingers in the left eye (OS) and 20/40 in the right (OD); intraocular pressures were normal bilaterally. Slit lamp examination revealed marked corneal edema, bullae, and central thinning with a deep anterior chamber OS. The right eye showed subtle inferocentral thinning without edema. Optical Coherence Tomography demonstrated extreme corneal swelling (central corneal thickness 2295 μm) and irregular keratometric rings OS, with early inferior steepening OD, which confirmed bilateral keratoconus with acute corneal hydrops OS. The patient was initiated on sodium chloride drops and ointment in both eyes, Cyclopentolate daily OS for pain, and artificial tears. At follow-up, the patient’s mother revealed a long-standing history of chronic eye rubbing due to allergic itching, which the patient had previously been unable to communicate. Olopatadine drops was prescribed for allergy control and strict eye-rubbing precautions were discussed. At one-week follow-up, pain and edema began to resolve and vision improved to 20/50 OS. The patient was informed that a preemptive corneal cross-linking procedure may benefit progression of currently mild keratoconus OD.

Discussion:
This case illustrates the importance of recognizing acute hydrops as an initial manifestation of keratoconus, thorough history-taking, and patient advocacy. In individuals with communication challenges, risk factors for keratoconus such as chronic eye rubbing may be overlooked. In this case, caregiver insight was essential in identifying allergies and eye rubbing as the root cause of the patient’s presentation, and allowed for targeted intervention. By initiating allergy control and behavioral counseling, progression of keratoconus was prevented in both eyes. This case highlights the value of early patient education and caregiver engagement, especially in vulnerable populations, to modify the trajectory of keratoconus and better preserve vision.

Acute Corneal Hydrops as the Initial Presentation of Keratoconus in a Young Adult

Background: Infections of the foot and ankle require prompt recognition and aggressive treatment to prevent complications such as osteomyelitis, nonunion, and limb-threatening deformity. In rare cases, fungal infections such as Phaeoacremonium venezuelense can lead to chronic osteomyelitis, posing significant reconstructive challenges. When extensive bone loss and joint destruction occur, traditional surgical options may not suffice. Recent advancements in 3D-printed implants have enabled limb salvage procedures in complex foot and ankle cases by offering patient-specific structural solutions. We present the first known case of midfoot reconstruction with a custom 3D-printed titanium cage following chronic P. venezuelense infection.

Case Presentation: A 56-year-old man with psoriatic arthritis initially presented in 2019 with right anterior ankle pain and was diagnosed with anterior tibial tendon tenosynovitis and synovitis. He underwent tendon repair and tenosynovectomy. Nine months later, following palm thorn trauma to the medial foot, the patient developed worsening pain, numbness in the 2nd and 3rd toes, and localized swelling. Subsequent imaging revealed first tarsometatarsal joint arthropathy with reactive bone marrow edema in the medial cuneiform and first metatarsal. Arthrodesis was performed, and intraoperative cultures confirmed P. venezuelense infection. Despite Voriconazole therapy and multiple surgeries, he developed chronic osteomyelitis and nonunion at the arthrodesis site. Amputation was recommended, but declined. Over two years, he underwent numerous debridements, skin grafts, methylmethacrylate spacer placements, and targeted antifungal regimens, including voriconazole, mycamine, amphotericin B, and isavuconazonium. Progressive bone loss necessitated cuboid and lateral column excision, resulting in midfoot-hindfoot discontinuity. After infection eradication was confirmed, a custom 3D-printed titanium cage packed with autograft harvested from the right proximal tibia was implanted. He progressed from non-weight-bearing to full ambulation, remaining pain-free with no sensory impairment or medication use at one-year follow-up. 

Discussion: This case report demonstrates the successful use of a custom 3D-printed titanium implant for limb salvage in chronic fungal osteomyelitis of the midfoot. Given the rarity and complexity of persistent P. venezuelense infections, traditional treatment options may not be sufficient, especially in patients with substantial bone deformity. Custom implants enabled an anatomic reconstruction for this patient after extensive bone loss, providing pain relief and restored function. This case supports 3D-printing as a viable option for complex foot and ankle reconstructions when standard interventions for chronic osteomyelitis fail. 


Complex Midfoot Reconstruction With 3D-Printed Titanium Cage Following Phaeoacremonium venezuelense Osteomyelitis

Tarsal tunnel syndrome (TTS), or posterior tibial neuralgia, is a neuropathy associated with compressive entrapment of the tibial nerve as it travels deep to the flexor retinaculum, or within the tarsal tunnel. The clinical signs and symptoms of a patient with TTS include: 1) painful burning, tingling, or numbness (paresthesia) sensations in the ankle the may extend distally into the toes or proximally to the knee; 2) inflammation of the feet; 3) abnormal temperature sensations within the feet; 4) electrical shock sensations due to impingement of the tibial nerve; and/or 5) patient complaints of lack of padding within the feet.1-5 These symptoms are exacerbated during physical activity or when a physician taps upon, or applies pressure to, the compressed tibial nerve, which is called a positive Tinel sign. Surgical incision of the flexor retinaculum of the foot usually relieves these TTS signs/symptoms because it creates additional space within the fibro-osseous passage for the impinged tibial nerve. Moreover, the presence of a variant leg muscle, the flexor digitorum accessorius longus (FDAL) muscle, has been implicated in TTS in that it can compress the tibial nerve along its course within the distal leg or by acting as a space-occupying structure within the tarsal tunnel as this supernumerary muscle passes deep to the flexor retinaculum. This muscular variant, which is present in 2-12% in cadaveric and imaging studies, should be ruled out before surgical incision of the flexor retinaculum, or these TTS signs/symptoms may persist.1,6-7 In this study of the FDAL muscle, novel distal insertions of this variant leg muscle were identified. We also describe the FDAL muscle in detail, share its anatomical relationship within the distal leg, and explain how the presence of this supernumerary muscle may predispose a patient to tarsal tunnel syndrome.

Novel distal insertions of flexor digitorum accessorius longus (FDAL) muscle and their implications on tarsal tunnel syndrome

Background
Ludwig’s Angina is a rapidly progressive and life-threatening cellulitis of the soft tissue of the floor of the mouth and neck. Streptococcal and Staphylococcal species are the most commonly isolated causes. It is treated with securing the airway, broad spectrum antibiotic coverage, and surgical drainage for any abscess or drainable collection of fluid. Sources of infection include dentition, oral procedures, alcoholism, vascular disease, and immunocompromised states. This is a case which was positive for Streptococcus Constellatus with systemic abscess spread and a 45-day ICU course. 

Methods
Case Report

Results
This is a 22-year old with diabetes, hypertension, asthma, hyperlipidemia, and alcohol use disorder. She reported poor dentition with dysphagia, drooling, pain in ears and throat for one week before arrival. She was seen at an urgent care four days prior and was given amoxicillin. Her oropharynx and tonsils were erythematous with tongue protrusion, dysphonia, poor dentition, diffuse swelling and induration noted to the submandibular area with tenderness to palpation with erythema with right side worse than left, and limited neck range of motion. She was intubated, started on broad spectrum antibiotics, and taken to the OR for an I&D of submental and submandibular abscesses. On day 6, OMFS removed five teeth. Chest tubes were inserted into the pleura and mediastinum for fluid collection, and repeat I&D procedures for the neck were performed. Abscess drainage on the right mastoid and a tympanostomy on the left were done. Spread to the cerebellum led to initiation of high dose ceftriaxone. Fluid studies from chest tube drainage and other wounds were negative. Her condition improved and was sent to a long-term acute care hospital.




Conclusion
This patient’s case shows complications found in Streptococcus Constellatus if not early controlled or immunosuppressed. Her Cushing’s Syndrome, steroid hormone therapy, and metabolic syndrome likely led to immunosuppression. These factors helped propagate the spread of abscesses to the CNS, mediastinum, lungs, and persistence of abscesses in mouth, neck, oropharynx, and mastoids. Early Pan CT in cases of Streptococcus Constellatus should be considered for its propensity to cause abscesses at distant sites, with early surgical evaluation of the mouth and neck. This patient’s difficulty of maintaining trough levels of vancomycin and not being on an antibiotic that was “sensitive” to this organism until day 4 after cultures resulted played a large role. Antibiotics providing double coverage for this organism would benefit patients like this as resistance continues to develop. 


Ludwig's Angina and a Complicated Course of Streptococcus Constellatus Management

Background
Treatment-resistant schizophrenia is defined by persistent delusions or hallucinations following failed trials of two other antipsychotic medications. Clozapine, an atypical antipsychotic medication approved by the FDA, is often the medication of choice in such challenging cases due to its proven efficacy. Its use is, however, tempered by a myriad of side effects which range from sedation, agranulocytosis, seizures, metabolic syndrome, and neuroleptic malignant syndrome. Mahendran R et. al particularly talked about clozapine being involved in the emergence or worsening of obsessive-compulsive symptoms (OCS) in up to 38.2% of patients, which is a side effect due to antagonism of the serotonin receptors 5-HT2A and 5-HT2C. On the other hand, tic-like vocalizations associated with clozapine are extremely rare and perhaps underreported.

Case Presentation
We describe a 39-year-old man with treatment-resistant schizophrenia and psychogenic polydipsia and Wolfe-Parkinson-White Syndrome s/p ablation, who, following the initiation and gradual titration of clozapine treatment, developed tic-like vocalizations and compulsive behaviors (excessive washing of face resulting in abrasions on forehead). While Clozapine was initially helpful in reducing some symptoms, the patient progressively developed treatment-emergent obsessive-compulsive behaviors and repetitive vocalizations. To manage these new challenges, a second antipsychotic medication, aripiprazole, was introduced in his regimen alongside intensive behavioral monitoring. Despite this, the vocalizations continued. A comprehensive evaluation ruled out any organic cause. This case illustrates the complex and treatment-resistant nature of these symptoms.

Discussion
Although clozapine-induced vocalizations are uncommon, they are a significant neuropsychiatric side effect that should be recognized by clinicians. Czapliński et al. described that vocalizations are characterized by sudden, repetitive, and stereotyped sounds, most commonly occurring hand in hand with compulsive behaviors or other movement symptoms. David D. Kim et al. explained in a systematic review that the response to adjunct therapies such as aripiprazole and behavior therapy can be helpful, and individualized treatment strategies are crucial. This case brings to light the importance of early identification and individualized treatment plans for atypical but meaningful side effects like clozapine-induced vocalizations. While clozapine is the treatment standard for treatment-resistant schizophrenia, its potential to cause or reveal obsessive-compulsive behavior and unusual vocalizations must be monitored carefully and addressed individually to maximize benefit with minimal risk of adverse effect.

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