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Unilateral Fixed Dilated Pupil - Differential Diagnosis Framework
If Altered Mental Status - Consider Oculomotor (3rd cranial
Unilateral Fixed Dilated Pupil - Differential Diagnosis Framework If Altered Mental Status - Consider Oculomotor (3rd cranial nerve) Palsy: • Brain (uncal) herniation, lntracranial hypertension, lntracranial hemorrhage, SAH, tumor • Posterior communicating artery aneurysm (Compression) If no neurological cause, consider: • Trauma • Medication effects • Congenital abnormalities #Unilateral #Fixed #Dilated #Pupil #differential #diagnosis #neurology
Transverse Myelitis Overview

Focal inflammatory disorder of the spinal cord resulting in rapid onset of weakness, sensory
Transverse Myelitis Overview Focal inflammatory disorder of the spinal cord resulting in rapid onset of weakness, sensory alterations, and bowel or bladder dysfunction Epidemiology: • 1400 new cases in the US each year • Bimodal peaks between the ages of 10 to 19 years and 30 to 39 years • 10-33% develop MS over a five to ten-year period • 75-90% of cases TM is monophasic Pathophysiology of Transverse Myelitis: • Excessive activation of an immune response against the spinal cord that results in CNS inflammation and tissue damage Mechanisms: • Idiopathic: etiology unknown • Infectious: Direct microbial infection versus molecular mimicry or super-antigen mediated disease • Immune Mediated Transverse Myelitis - Clinical Presentation: Injury to the spinal cord (Myelopathy) without cord compression (MRI) and findings of varying degrees of: 1. Weakness: - Weakness that preferentially affects the flexors of the legs and the extensors of the arms (pyramidal distribution of weakness) - Flaccidity -> Spasticity - Reflexes: decreased or absent initially -> Hyperreflexia develops later 2. Sensory Alterations: - Sensory features: paresthesias ascending from feet with or without back pain at/near level of myelitis 3. Autonomic Dysfunction: - Autonomic: Bowel/Bladder dysfunction, temperature dysregulation, bouts of HTN Diagnostic Criteria: • Sensory, motor, or autonomic dysfunction located at the spinal cord • T2 hyperintense signal change on spinal MRI • No evidence of compressive cord lesion • Bilateral signs and/or symptoms • Clearly defined sensory level • CSF inflammation: CSF pleocytosis, elevated IgG index • Progression hours to days Transverse Myelitis Diagnosis: • Must rule out compressive myelopathies! • Gadolinium-enhanced MRI of the spinal cord - Increased T2 signal and expansion of the cord - No cord compression - More than 2/3 of the cross-sectional area is involved - Focal enlargement - T2WI hyperintensity - Enhancement - TM and tumor the cord is swollen, while in MS and ADEM the cord is not swollen or less swollen - Lesion > 3 levels: Evaluate for NMO, SLE or Sjogren's • CSF: - Abnormal in 50% of cases - Pleocytosis: Mild lymphocytic - Pleocytosis > 100 cells: consider infectious myelitis - Elevated IgG index - Oligoclonal IgG bands (85 to 95% Predictive of MS) • Check Vitamin B12 and copper levels • NMO-IgG (anti-AQP4) should be tested and if negative, MOG-IgG test should be ordered • Infectious causes need to be ruled out • Brain MRI: Check for brain and/or optic nerve lesions suggestive of multiple sclerosis, NMOSD, MOG antibody disorders, or ADEM Transverse Myelitis Etiologies: • Demyelination: - Multiple sclerosis (MS) - Neuromyelitis optica (NMO) - Idiopathic transverse myelitis - ADEM - Post vaccination - Myelin oligodendrocyte glycoprotein (MOG) antibody disorders • Infections: - Herpes zoster, West Nile virus - Herpes simplex virus, HIV, Hep A/B/CMV, TB - Treponema Pallidum - Lyme Disease Mycoplasma - Leptospirosis, Brucellosis - Dengue, EBV, Influenza, Enteroviruses • Idiopathic: - Post Infectious - Post Vaccine • Inflammatory Disorders: - SLE - Neurosarcoidosis - MCTD - Bechet disease - Sjogren - Vasculitis- Heroin • Paraneoplastic: - AntiGAD65, NMDAR, AntiCRMP IgG, Anti-Hu - Antiamphiphysin antibodies • Nutritional Deficiency: - Vitamin B12, E, D, copper Transverse Myelitis Treatment: • Steroids • Plasma exchange • Immunomodulatory agents: IVIG • Cyclophosphamide #Transverse #Myelitis #diagnosis #management #neurology #differential
Tinnitus - Subjective (heard only by patient) - 90% - Differential Diagnosis Algorithm
Unilateral On Audiogram -
Tinnitus - Subjective (heard only by patient) - 90% - Differential Diagnosis Algorithm Unilateral On Audiogram - Perform MRI to rule out RC Lesion • Acoustic Neuroma • Lesion of Cochlear or Auditory Nerve • Brainstem Lesion • Multiple Sclerosis • Infarction • Méniére's Disease Bilateral - No Hearing Loss: • Metabolic Causes: Thyroid Dysfunction, Vitamin A, B, Zinc Deficiency. • Psychogenic, Anxiety, Depression • Drugs (Salicyclates, Quinidine, Indomethacin) • Idiopathic Bilateral - Conductive Hearing Loss: • Lesion of External or Middle Ear • Impacted Cerumen • Otitis Media • Otosclerosis Bilateral - Sensorineural Hearing Loss: • Noise Induced • Ototoxicity • Presbycusis • Drugs (Propranolol, Levodopa, Loop Diuretics) • Congenital Somatic: • TMJ • Bruxism • Whiplash • Skull Fracture • Closed Head Injury #Tinnitus #Ringing #hearing #subjective #Differential #Diagnosis #Algorithm #Causes
Thiamine Deficiency - Differential Diagnosis Framework and Clinical Manifestations

Causes of Thiamine Deficiency:
 • Poor intake:
	- Diets
Thiamine Deficiency - Differential Diagnosis Framework and Clinical Manifestations Causes of Thiamine Deficiency: • Poor intake: - Diets high in polished rice/processed grains - Chronic alcoholism - TPN - Gastric bypass surgery • Poor absorption: - Malnutrition - Gastric bypass surgery - Malabsorption • Increased loss: - Diarrhea - Hyperemesis gravidarum - Diuretic use - Renal replacement therapy • Increased thiamine utilization: - Pregnancy - Lactation - Hyperthyroidism - Refeeding syndrome Sources of Thiamine: • Found in: Yeast, Legumes, Pork, Brown rice, Cereals • Low in: White/polished rice, Milled white cereals, Milk products Thiamine • Necessary For: - Oxidative phosphorylation - Myocardial energy production • Deficiency leads to increased pyruvate and lactate • Increased pyruvate & lactate decrease PVR and increase venous blood flow, increasing cardiac preload • Increased preload and myocardial dysfunction leads to congestive heart failure • Wet beri-beri triggers Right HF • Moderate pulmonary HTN is common • Hyperkinetic LVEF is also seen • Lactic acidosis may not demonstrate diminished pH due to compensatory hyperventilation Wernicke-Korsakoff Syndrome: • Wernicke's Encephalopathy - Acute neurological condition: - Nystagmus - Ophthalmoplegia - Ataxia/confusion - WE + memory loss & psychosis with confabulation is consistent with WKS • Korsakoff Syndrome - Chronic neurological condition: - Impaired short-term memory - Confabulation Beri Beri: • Dry Beri Beri: - Symmetrical peripheral neuropathy of the distal extremities - Sensory and motor impairments - Impaired reflexes - Burning pain in extremities - Muscle weakness - Falls due to peripheral neuropathy • Wet Beri Beri: - High output heart failure - Dilated cardiomyopathy - Tachycardia - High output congestive HF - Peripheral edema Additional Findings: • Acute renal failure: - Increased Lactate/Pyruvate - AV shunt, renal vascular contraction, blood flow reduction - Decreased GFR • Acute liver failure: Hepatic congestion due to RHF #Thiamine #Deficiency #Manifestations #Differential #Diagnosis #syndromes #beriberi #nutrition #pathophysiology #wernickes #korsakoff
Syncope in 3 Steps
1. Consider the 3 "S" Mimics: Seizure, low Sugar, Stroke (TIA)
2. Heart vs
Syncope in 3 Steps 1. Consider the 3 "S" Mimics: Seizure, low Sugar, Stroke (TIA) 2. Heart vs SVR Heart • Pump > AS, HOCM, PE, pHTN, Tamponade • Fluid > low like Gl loss, shunting like subclavian steal syndrome • Rhythm > fast or slow SVR • Too much para > vasovagal, situational, carotid hypersensitivity and others <3 • Too little sympa > meds, diabetes, Parkinson (+), AL amyloidosis and other #Syncope #differential #diagnosis #mimics
Stiff Person Syndrome (SPS) - Diagnosis and Management Summary

Epidemiology:
 • Prevalence: 1-2 cases per million -
Stiff Person Syndrome (SPS) - Diagnosis and Management Summary Epidemiology: • Prevalence: 1-2 cases per million - rare • Age 20-50, Females 2-3 times than men • Commonly associated with DM-1, thyroiditis, vitiligo, and pernicious anemia Stiff Person Syndrome Pathophysiology: • Associated with autoimmunity • Research indicates that it is the result of an autoimmune response gone awry in the brain and spinal cord. Clinical Manifestations of Stiff Person Syndrome: • Progressive muscle stiffness, rigidity, spasm - axial muscles • Severely impaired ambulation • Excessive muscle rigidity - lumbar, trunk, proximal muscles - sustained muscle contractions (agonist and antagonist muscles) • Wide based gait with tendency to fall • Triggers - sudden movement, noise, emotional upset • Spasms - visualized-tight, rock-hard, board-like feel • Autonomic dysfunction - hyperpyrexia, diaphoresis, high HR • Sudden death - diaphragm spasm - apnea Stiff Person Syndrome - Diagnosis: • High index of suspicion • Presence of: - Stiffness in axial and limb muscles resulting in impairment of ambulation - Presence of superimposed spasms triggered by noise, movement or emotions - A positive therapeutic response to diazepam or findings of continuous motor unit activity on EMG - Absence of other neurological disorders • Testing anti-GAD (positive in 2/3 of pts) • Therapeutic trial of diazepam • EMG testing Lab Findings in Stiff Person Syndrome: • Anti-GAD Ab (>1000u/ml) - People with SPS have elevated levels of GAD, an antibody that works against an enzyme involved in the synthesis of an important neurotransmitter in the brain. • CSF: Oligoclonal bands • Normal ESR, CRP • Other autoantibodies - TPO, TTG, etc EMG Studies: • Continuous motor-unit activity, typically decreased by diazepam, sleep DDx: • Neuromyotonia, Tetanus, Strychnine poisoning, Parkinson's disease, Multiple sclerosis, Ankylosing spondylitis, Axial dystonia, Focal limb or joint disorders, Fibromyalgia, Psychosomatic illness, Anxiety, Phobia Stiff Person Syndrome Treatment: • Initial/Symptomatic Therapy: - BDZ: Diazepam or clonazepam • Resistant to Initial Symptomatic Therapy: - Baclofen • Severe Disease/Resistant: - IVIG - If Resistant to IVIG: Rituximab (anti-CD20), plasma exchange, or others (botox, sodium valproate, vigabatrin, propofol) #Stiff #Person #Syndrome #SPS #Diagnosis #Management #treatment #neurology
Pupils: Localization in Coma
 • Small, Reactive pupils: Metabolic coma.
 • Unilateral Fixed, dilated pupil :
Pupils: Localization in Coma • Small, Reactive pupils: Metabolic coma. • Unilateral Fixed, dilated pupil : uncal herniation, PCOM aneurysm. • Bilateral, Large fixed pupils: Midbrain lesion or Death. • Bilateral, midposition, fixed pupils: Transtentorial herniation. • Pinpoint pupils: Pontine ICH, infarct, Opiate poisoning. • Horner's syndrome: sympathetic dysfunction. #Pupils #Localization #Coma #Neurology #differential #diagnosis
Ptosis - Differential Diagnosis Framework

Ptosis (Greek- to fall) Drooping of the upper eyelid that usually results
Ptosis - Differential Diagnosis Framework Ptosis (Greek- to fall) Drooping of the upper eyelid that usually results from a congenital or acquired abnormality of the muscles that elevate the eyelid. When patients present with ptosis, it is important to think about three clinical diagnoses associated with ptosis: 1. CN III palsy 2. Horner’s syndrome 3. Myasthenia gravis Neurogenic Ptosis - Neurologic disease affecting the muscle, neuromuscular junction, cranial nerve, and the brainstem may lead to ptosis and weakness of the levator muscle of the upper eyelid: • Third nerve palsy • Horner syndrome • Myasthenia gravis • Botulinum toxin • Multiple sclerosis • Cerebral ptosis - Supranuclear lesions • Ophthalmoplegia migraine Myogenic Ptosis: • Mitochondrial myopathy • Myotonic dystrophy • Myasthenia gravis • Ocular myopathy • Oculopharyngeal muscular dystrophy • Blepharophimosis syndrome Aponeurotic Ptosis: • Spontaneous disinsertion or dehiscence of the levator aponeurosis (the tendon connecting the levator to the tarsal plate) • Involutional (senile) change • Contact lens wearing • Ocular surgery Congenital Ptosis - Absence or reduction of striated levator palpebrae superioris muscle: • Marcus Gunn jaw-winking syndrome Traumatic Ptosis - Direct or indirect trauma to the eyelid leading to: • Levator transection • Cicatrization • Eyelid laceration or orbital rooftop fracture with ischemia Mechanical Ptosis - Levator function is impaired due to the mass effect of some abnormal external structure/excess weight on the upper lid: • Neoplasm • Chalazion • Contact lens in the upper fornix • Scarring • Ocular pemphigoid • Trachoma Pseudoptosis: • Microphthalmos • Anophthalmos • Enophthalmos • Lid retraction of one eye causing ptosis in the contralateral eye • Redundant eyelid skin and prolapse of the orbital fat (dermatochalasis) • Lowering the ipsilateral eyebrow and raising the contralateral one • Duanes Syndrome #Ptosis #neurology #Differential #Diagnosis #ophthalmology #ocular
Posterior Reversible Encephalopathy Syndrome (PRES) Overview

Clinico-Radiological Syndrome, characterized by:
 • Headache
 • Seizures
 • Altered mental
Posterior Reversible Encephalopathy Syndrome (PRES) Overview Clinico-Radiological Syndrome, characterized by: • Headache • Seizures • Altered mental status • Visual disturbance • White matter vasogenic edema affecting the posterior occipital and parietal lobes of the brain PRES Clinical Presentation: • Altered mental status • Headache • Seizures • Vision changes • Hypertensive crisis may precede the neurologic syndrome by 24 hours or longer/BP fluctuations PRES-Associated Clinical Conditions: • Preeclampsia, Eclampsia, Infection/Sepsis/Shock, Autoimmune disease, Cancer chemotherapy, Immunosuppressive agents, Renal failure, Transplantation including bone marrow or stem cell transplantation, Hypertension/Hypertensive emergency, Blood transfusion, Hypercalcemia Etiology: • Pathophysiology remains unclear, endothelial dysfunction is key, with hypertension being the most common precipitating factor PRES Diagnosis: 1. Neurological symptoms: Acute onset 2. Risk factors 3. Imaging Patterns in PRES: • Increased signal on T2-weighted images • Vasogenic edema visualized as a hypo- or isointense signal on DWI • White matter edema - both posterior cerebral hemispheres • (FLAIR) sequences improve sensitivity showing cortical lesions • Vascular narrowing on MRA/CTA • Anterior circulation: MCA ACA watershed territories signal changes 4. Reversible course Differential Diagnosis: • Infection, Electrolyte abnormality, Medication/Drug toxicity, Metabolic disturbance, External lines/devices, Constipation, Seizures, Stroke, Paraneoplastic syndrome, ADEM, Acute toxic leukoencephalopathy, Cerebral venous thrombosis Testing: • Imaging: White matter vasogenic edema affecting the posterior occipital and parietal lobes of the brain • CSF: Modestly elevated protein level (mean 58 mg/dL in one study) but no pleocytosis. An elevated white blood cell count in the CSF should prompt consideration of other diagnoses. • EEG: With persistent altered level of consciousness to exclude nonconvulsive status epilepticus Treatment: • Address the underlying cause • Treatment of HTN is the mainstay of therapy in patients - 10-25% BP reduction initially, Avoid overaggressive BP lowering - Lower the diastolic pressure to 100-105 mmHg within 2 to 6 hours - Use easily titratable parenteral agents: clevidipine, nicardipine, or labetalol. • Magnesium correction: Levels 2-3 mEq/L • Seizures: Treat with AEDs until cause identified #PRES #Posterior #Reversible #Encephalopathy #Syndrome #diagnosis #management #neurology
Photophobia and Headache - Differential Diagnosis Framework

Why?
• The coexistence of photophobia and headache suggests the potential
Photophobia and Headache - Differential Diagnosis Framework Why? • The coexistence of photophobia and headache suggests the potential reciprocal interactions between visual and pain pathways. • Interactions between visual and pain pathways occur at the retina, midbrain, thalamus, hypothalamus, and visual cortex. • In migraines: photophobia could result from photic activation of retina-driven pathways involved in the regulation of homeostasis. Primary headaches: • Migraine: - 80 percent of people who have migraines have photophobia - Bilateral photophobia - Severe persistent photophobia - Migraine with aura > migraine without aura - Chronic migraine > episodic migraine - Benign episodic mydriasis, miosis • Tension-type headache: - Bilateral or unilateral photophobia - Mild persistent photophobia • Trigeminal autonomic cephalalgias (TACs): - Hemicrania continua, SUNCT, SUNA, etc. - Unilateral - Reversible, only during their cluster period - Moderate, between migraine and tension-type headache - Autonomic symptoms - Miosis Secondary headaches: • Traumatic brain injury (TBI): - Reversible or persistent photophobia • Meningitis: - Patients tend to have meningeal irritation signs - Photophobia in viral meningitis is the most common form • Non-traumatic subarachnoid hemorrhage (SAH): - Mydriasis - Can have isolated photophobia without headache • Disorder of the eyes - Photophobia often precedes the onset of headache: - Acute angle-closure glaucoma - Ocular inflammatory disorder - Trochlear headache • CNS Vasculitis Painful cranial neuropathies: • Trigeminal neuralgia: - Common in patients with the first division of the trigeminal nerve pain - Mydriasis • Painful optic neuritis #Photophobia #Headache #differential #diagnosis #ophthalmology #Neurology