Neurological Side Effects of Antipsychotic Drugs Acute dystonia - Spasm of muscles of tongue, face, neck, back • Time: 1-5 days. Young, antipsychotic, naive patients at highest risk • Tx: Antiparkinsonian agents are diagnostic and curative Akathisia - Subjective and objective restlessness; not anxiety or "agitation" • Time: 5-60 days • Tx: Reduce dose or change drug; clonazepam, propranolol more effective than antiparkinsonian agents Parkinsonism - Bradykinesia, rigidity, variable tremor, mask facies, shuffling gait • Time: 5-30 days. Elderly at greatest risk • Tx: Dose reduction; change medication; antiparkinsonian agent Neuroleptic malignant syndrome - Extreme rigidity, fever, unstable blood pressure, myoglobinemia; can be fatal • Time: weeks-months. Can persist for days after stopping antipsychotic • Tx: Stop antipsychotic immediately; supportive care; dantrolene and bromocriptine Perioral tremor ("rabbit syndrome") - Perioral tremor (may be a late variant of parkinsonism) • Time: months or years of treatment • Tx: Antiparkinsonian agents often help Tardive dyskinesia - Orofacial dyskinesia; rarely widespread choreoathetosis or dystonia • Time: months or years of treatment. • Tx: May be reversible with early recognition and drug discontinuation VMAT2 inhibitors valbenazine and deutetrabenazine are FDA-approved for TD #Antipsychotic #Drugs #Medications #SideEffects #pharmacology #management

Serotonin Syndrome - Rapid onset - Combination of 2+ serotonin agonists Mental status changes: - Agitation - Pressured speech Autonomic instability: - Tachycardia - Diarrhea - Shivering - Diaphoresis - Mydriasis Neuromuscular abnormalities: - Clonus - Hyperreflexia (lower > upper) - Tremor - Seizure Rx: - Benzodiazepines - Hydration/Cooling - Cyproheptadine #Serotonin #Syndrome #Diagnosis #Management

Algorithm and Differential Diagnosis of Tremor #Diagnosis #IM #PrimaryCare #Neuro #Tremor #Action #Rest #Differential #Algorithm #Comparison #Table #Ddxof

Wave changes during evolution of myocardial damage. #Pathophysiology #Cardiology #EKG #Evolution #Infarct #Ischemia

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