Neurology Patient Cases PDF

Neurology Patient Cases (Cont’d) 24. M.K. is a 44-year-old woman with right-sided headaches of moderate intensity that are accompanied by severe nausea and vomiting. Which medication would be best for M.K.’s migraine headaches? A. Almotriptan. B. Naratriptan. C. Promethazine. D. Sumatriptan. 25. ...

Neurology Patient Cases (Cont’d) 24. M.K. is a 44-year-old woman with right-sided headaches of moderate intensity that are accompanied by severe nausea and vomiting. Which medication would be best for M.K.’s migraine headaches? A. Almotriptan. B. Naratriptan. C. Promethazine. D. Sumatriptan. 25. T.C. is a 30-year-old woman with migraine headaches. Sumatriptan 100 mg provides immediate relief. However, about 2 hours later, her headache symptoms return. Which would be best for her? A. Rizatriptan 5 mg. B. Frovatriptan 2.5 mg. C. Naproxen 250 mg. D. Topiramate 25 mg. V. MULTIPLE SCLEROSIS A. Definitions 1. Autoimmune disorder with areas of CNS demyelination and axonal transaction 2. Clinical course a. Clinically isolated syndrome; first clinical presentation for which the 2017 diagnostic criteria for MS have not been met b. Classified as relapsing-remitting, secondary progressive, and primary progressive, with subclassification according to disease activity and progression: Relapsing-remitting: 85% of patients at diagnosis, develops into progressive disease in 50% of patients within 10 years B. Epidemiology 1. Diagnosis is usually at 20–50 years of age. 2. Twice as many women as men develop MS. 3. White people and people of northern European heritage are more likely to develop MS. 4. Risk factors: Family history of MS, autoimmune disease, or migraine; personal history of autoimmune disease or migraine; cigarette smoke exposure, obesity (especially in childhood and adolescence), vitamin D deficiency, geography, genetic factors, Epstein-Barr virus C. Treatment 1. Acute relapses are treated with high-dose corticosteroids. a. Intravenous methylprednisolone: Usual dose is 500 mg to 1 g daily for 3–7 days (5 days typically), either alone or followed by an oral taper with prednisone. b. Oral prednisone: Usual dose is 1250 mg/day administered every other day for five doses. c. Intravenous adrenocorticotropic hormone d. Neurologic recovery is the same with or without an oral prednisone taper. 2. Disease-modifying therapies (Table 9) a. Alemtuzumab (Lemtrada) i. Mechanism of action: Binds to CD52, a cell surface antigen on T cells, B cells, natural killer cells, monocytes, and macrophages; causes lysis of T and B cells ACCP Updates in Therapeutics® 2023: The Pharmacotherapy Preparatory Review and Recertification Course 1-520 Neurology ii. Adverse effects (a) Autoimmunity, including thyroid disorders (34%), immune thrombocytopenia, glomerular nephropathies (b)  Infusion reactions (e.g., anaphylaxis, angioedema, bronchospasms, nausea, urticaria) occur in up to 92% of patients and necessitate corticosteroids during treatment. (c) Increased infections: Screen for herpes zoster and immunize, if needed; screen for tuberculosis before initiating therapy; prophylaxis for herpes infections is necessary during treatment. (d) May increase the risk of thyroid cancer, melanoma, and lymphoma (e) Administered only under a restricted distribution program iii. Avoid live virus vaccines during treatment; complete all vaccines 6 weeks before initiating therapy. iv. Avoid pregnancy during treatment and for 4 months after each treatment course. b. Beta-interferons (Avonex, Betaseron, Extavia, Plegridy, Rebif) i. Mechanism of action: Suppress T-cell activity, down-regulate antigen presentation by major histocompatibility complex class II molecules, decrease adhesion molecules and matrix metalloproteinase-9, increase anti-inflammatory cytokines, and decrease inflammatory cytokines ii. Adding polyethylene glycol to interferon beta-1a decreases the frequency of injections. iii. Injection site reactions: More common in subcutaneously administered products. May help to bring a drug to room temperature before injection, ice the injection site, and rotate injection sites iv. Flu-like symptoms: Usually dissipate in 2–3 months. May help to inject the dose in the evening. Begin at the 0.25- to 0.5-mg dose and slowly increase, and use ibuprofen or acetaminophen. v. Neutralizing antibodies: Develop in some patients 6–18 months after treatment begins; frequency and administration route affect neutralizing antibody development; relapse rates are higher in patients with persistently high antibody titers; antibodies may disappear even during continued treatment; show cross-reactivity with other beta-interferons vi. Avoid in severe, untreated depression. c. Dimethyl fumarate (Tecfidera) i. Mechanism of action: Antioxidant and cytoprotective; inhibits proinflammatory cytokines, increases anti-inflammatory cytokines ii.  Adverse effects (a) Skin flushing: Occurs in up to 38% of patients, usually within 30–45 minutes of dosing; involves the face, chest, and neck; dissipates after 15–30 minutes; peaks within first month of therapy and decreases thereafter; aspirin may block flushing, taking with food helps prevent (b) GI events: Occur in up to 41% of patients; peak within first month of therapy and decrease thereafter (c) Lymphocytes decrease by 30% in the first year of therapy and then stabilize. (d) Hepatotoxicity onset ranging from a few days to months after treatment initiation. Liver function test abnormalities resolve after therapy discontinuation. iii. Indicated for use in pregnancy d. Glatiramer acetate (Copaxone) i. Mechanism of action: Decreases type 1 helper T cells; increases type 2 helper T cells; increases production of nerve growth factors ii. Injection site reactions: Icing the site before and after injection and rotating the injection site may help. iii. Systemic reactions: May involve flushing, chest tightness, palpitations, anxiety, and shortness of breath; this is noncardiac; recurrence is infrequent iv. Avoid use in pregnancy unless clearly needed. ACCP Updates in Therapeutics® 2023: The Pharmacotherapy Preparatory Review and Recertification Course 1-521 Neurology e. Fingolimod (Gilenya) i. Mechanism of action: Binds to the sphingosine-1-phosphate receptor 1, 3, 4, 5 expressed on T cells, prevents activation of T cells ii. Indicated for patients 10 years and older iii. Contraindicated in patients with myocardial infarctions, unstable angina, stroke, TIAs, or decompensated heart failure necessitating hospitalization or class III/IV heart failure, history of Mobitz type II second- or third-degree atrioventricular block or sick sinus syndrome unless patient has a pacemaker, baseline QTc interval of 500 milliseconds or greater, or treatment with class Ia or class III antiarrhythmic drugs iv. Patients must be monitored for bradycardia for 6 hours after the first dose; if therapy is discontinued for more than 2 weeks, patients must be re-monitored. v. Adverse effects (a) Bradycardia: ECG is recommended within 6 months for patients using antiarrhythmics (including β-blockers and calcium channel blockers), those with cardiac risk factors, and those with a slow or irregular heartbeat. Heart rate returns to baseline within 1 month of continued dosing. (b) Atrioventricular conduction delays: First- and second-degree block (c) Decrease in lymphocytes: A recent CBC should be available before therapy begins. Infections may be more common. Discontinue therapy for serious infections; test patients without varicella zoster vaccine or infection history for varicella zoster virus antibodies, and immunize antibody-negative patients (wait 1 month to initiate fingolimod). (d) Macular edema: Ophthalmologic evaluation at baseline and 3–4 months after fingolimod initiation; a history of uveitis or diabetes increases risk (e) Respiratory effects: Decreases in forced expiratory volume in 1 second and diffusion lung capacity for carbon monoxide can occur. (f)  Elevation of liver enzymes (g)  Hypertension: Monitor during treatment. (h) Extended effects of drug for up to 2 months after discontinuation necessitate extended monitoring for many adverse effects. vi. Drug interactions (a) Ketoconazole: Increased fingolimod (b) Vaccines: Less effective during and 2 months after fingolimod treatment; avoid live-attenuated vaccines vii. Avoid pregnancy during treatment and for 2 months after treatment. viii. Medication guide required f. Mitoxantrone (Novantrone) i. Mechanism of action: Decreases monocytes and macrophages, inhibits T and B cells ii. Indicated for secondary progressive, primary progressive, and worsening relapsing-remitting MS; used infrequently because of toxicity iii. Because of the potential for toxicity, mitoxantrone is reserved for patients with rapidly advancing disease whose other therapies have failed. iv. Patients taking mitoxantrone should not receive live virus vaccines; other vaccines should be held for 4–6 weeks after dose. v. Cardiotoxicity: Echocardiograms or multigated acquisition scans must be done at baseline and before each infusion. Systolic dysfunction occurs in about 12% of patients; congestive heart failure occurs in about 0.4%. Cardiotoxicity is not related to dose, sex, or age. Cyclooxygenase 2 inhibitors should be avoided; cumulative lifetime maximum dose of 140 mg/m2 ACCP Updates in Therapeutics® 2023: The Pharmacotherapy Preparatory Review and Recertification Course 1-522 Neurology vi. Therapy-related acute leukemia occurs in about 0.8% of patients. vii. Other laboratory tests (CBC, bilirubin, AST, ALT, ALP, and pregnancy test) must be done before each infusion. viii. Avoid pregnancy during treatment. g. Natalizumab (Tysabri) i. Mechanism of action: Blocks T-cell entry into the CNS ii. Indicated for relapsing forms of MS but distributed through restricted distribution program because of progressive multifocal leukoencephalopathy risk (0.24%) iii. Adverse effects (a) Hypersensitivity reactions: Itching, dizziness, fever, rash, hypotension, dyspnea, chest pain, anaphylaxis, usually within 2 hours of administration (b) Progressive multifocal leukoencephalopathy: Rapidly progressive viral CNS infection; usually results in death or permanent disability. Patient selection guidelines are for patients with relapsing-remitting disease whose other treatment (efficacy or intolerability) has failed or who have an aggressive initial course; should not be used in combination with other disease-modifying therapies. On January 20, 2012, an FDA-issued drug safety communication stated that positive tests for John Cunningham virus (JCV) antibodies were a risk factor for progressive multifocal leukoencephalopathy. Thus, patients with all three of the following risk factors – presence of anti-JCV antibodies, longer natalizumab treatment duration (especially beyond 2 years), and previous treatment with an immunosuppressive medication (mitoxantrone, azathioprine, methotrexate, cyclophosphamide, mycophenolate mofetil) – have a 1.1% chance of developing progressive multifocal leukoencephalopathy. (c) Antibodies to natalizumab, associated with increased relapses and hypersensitivity reactions, develop in 9%–12% of patients. (d) Severe liver toxicity, depression (e) Recent analysis found natalizumab may be used during pregnancy with patients at severe risk of disease reactivation during pregnancy. (f) REMS program required because of risk of progressive multifocal leukoencephalopathy associated with natalizumab h. Ocrelizumab (Ocrevus) i. Mechanism of action: Thought to bind to CD20 on pre-B and mature B cells ii. Indicated for relapsing or primary progressive forms of MS iii.  Pharmacokinetics: Two-compartment model with central compartment volume 2.78 L. Terminal half-life 26 days iv. Adverse effects (a) Infectious: Respiratory infections, herpes virus infections (b) Psychiatric: Depression (c) Infusion reactions (d) GI: Diarrhea (e) Malignancies v. Must test for hepatitis B before first dose, contraindicated if positive vi. Premedicate with methylprednisolone and an antihistamine before each infusion. vii. Administer necessary vaccines 4 weeks before dose (live, live-attenuated) or 2 weeks before dose (non-live). viii. Avoid pregnancy during treatment and for 6 months after treatment. ACCP Updates in Therapeutics® 2023: The Pharmacotherapy Preparatory Review and Recertification Course 1-523 Neurology i. Ofatumumab (Kesimpta) i. Mechanism of action: Selectively targets and binds cell surface antigen CD20 on B cells, resulting in their depletion ii. Indication: Relapsing-remitting MS and secondary progressive disease iii. Contraindication: Active hepatitis B virus infection iv. Adverse effects: (a) Hepatitis B reactivation (b) Infection (upper respiratory tract infection)/reduction in immunoglobulins (c) Injection-related reactions – localized and systemic (d) Headache v. Avoid pregnancy during treatment and for 6 months after treatment. j. Ozanimod (Zeposia) i. Mechanism of action: Sphingosine-1-phosphate receptor modulator ii. Indicated for relapsing forms of MS, including clinically isolated syndrome, relapsing-remitting, and active secondary progressive disease iii. Dose: Titrate dose to maintenance dose of 0.92 mg orally daily. iv. Contraindications: Within the past 6 months, patient has experienced a myocardial infarction, unstable angina, stroke, TIA, decompensated heart failure with hospitalization, class III or IV heart failure, Mobitz type II second-degree heart block, third-degree atrioventricular block, sick sinus syndrome, sinoatrial block, unless a functioning pacemaker v. Adverse effects: Increased risk of infection, bradyarrhythmia and atrioventricular conduction delays, hepatotoxicity, teratogenicity, hypertension, decreased pulmonary function, macular edema, orthostatic hypotension vi. Drug interactions: Avoid CYP2C8 inducers and inhibitors, BCRP inhibitors, and live-attenuated vaccinations. vii. Avoid pregnancy during treatment and for 3 months after treatment. k. Ponesimod (Ponvory) i. Mechanism of action: Sphingosine-1-phosphate receptor modulator ii. Indicated for treatment of relapsing forms of MS (including clinically isolated syndrome), relapsing-remitting disease, and active secondary progressive disease in adults iii. Dose (a) Initial: Administer once daily according to the 14-day dose titration shown in Table 8. Table 8. Ponesimod Initial Dosage Titration Day of Therapy 1 and 2 3 and 4 5 and 6 7 8 9 10 11 12, 13, and 14 15 and thereafter Dose (mg) 2 3 4 5 6 7 8 9 10 20 (b) Maintenance: 20 mg once daily, beginning on day 15 ACCP Updates in Therapeutics® 2023: The Pharmacotherapy Preparatory Review and Recertification Course 1-524 Neurology iv. Contraindications (a) In the past 6 months, patient has experienced myocardial infarction, unstable angina, stroke, TIA, decompensated heart failure requiring hospitalization, or class III or IV heart failure (b) Presence of Mobitz type II second-degree, third-degree atrioventricular block, or sick sinus syndrome, unless patient has a functioning pacemaker v. Drug interactions: Avoid immunosuppressive drugs and live vaccinations. vi. Adverse reactions (a) Transient, dose-dependent bradycardia; first-degree atrioventricular block; and hypertension have been observed primarily after the first dose of ponesimod and with dose titration. (b) Cutaneous malignancies are rare. (1) Basal cell carcinoma (2) Malignant melanoma (3) Squamous cell carcinoma (c) Hepatotoxicity (d) Increased risk of infection (e.g., upper respiratory tract, urinary tract, viral infections [herpes]) vii. Avoid pregnancy during treatment and for 1 week after treatment. l. Teriflunomide (Aubagio) i. Mechanism of action: Prevents activation of lymphocytes ii. Indicated for relapsing forms of MS iii. Pharmacokinetics: Long half-life (18–19 days); takes about 3 months to reach steady-state concentrations; takes an average of 8 months to eliminate drug (serum concentrations less than 0.02 mcg/mL) and may take up to 2 years iv. Adverse effects (a) Hepatotoxicity may occur; teriflunomide should not be used in patients with preexisting liver disease or with ALT more than 2 times the upper limit of normal. Discontinue if severe liver damage occurs. (b) GI effects: Diarrhea, nausea (c) Dermatologic effects: Alopecia, rash (Stevens-Johnson syndrome) (d) Infection: Neutropenia and lymphopenia may occur; tuberculosis infections reported (negative tuberculosis skin test required at baseline); live virus vaccinations should not be administered (e) Teratogenic: Contraindicated in women of reproductive potential; negative pregnancy test at baseline; adequate contraception should be ensured; if pregnancy is desired for men or women, teriflunomide should be discontinued, accelerated elimination procedures should be undertaken, and two serum concentrations less than 0.02 mcg/mL taken 14 days apart should be confirmed v. Accelerated elimination procedures (a) Cholestyramine 8 g every 8 hours for 11 days (if not tolerated, may use 4 g) (b) Activated charcoal powder 50 g every 12 hours for 11 days m. Siponimod (Mayzent) i. Mechanism of action: Sphingosine-1-phosphate receptor modulator, blocking the ability of lymphocytes to leave lymph nodes and enter systemic circulation ii. Indication: Clinically isolated syndrome; relapsing forms of MS, including relapsing-remitting; and active secondary progressive disease ACCP Updates in Therapeutics® 2023: The Pharmacotherapy Preparatory Review and Recertification Course 1-525 Neurology iii. Adverse effects (a) Common: Headache, hypertension, increased liver function tests (b) Serious: Infections, macular edema, bradyarrhythmia, atrioventricular conduction delays, decreased pulmonary function, hepatotoxicity iv. Contraindications: (a) CYP2C9*3*3 genotype (b) Myocardial infarction, unstable angina, stroke, TIA, decompensated heart failure, class III/IV heart failure in the past 6 months (c) Mobitz type II second-degree, third-degree atrioventricular block, sick sinus syndrome v. Drug interactions (a) Avoid live-attenuated vaccines during and up to 4 weeks after treatment. (b) CYP2C9 and CYP3A4 moderate or strong inhibitors and inducers should be avoided. vi. Avoid pregnancy during treatment and for 10 days after treatment. n. Cladribine (Mavenclad) i. Mechanism of action: Not established for MS, but may be the result of cytotoxic effects on B and T lymphocytes ii. Indication: Relapsing forms of MS, including relapsing-remitting and active secondary progressive disease iii. Adverse effects (a) Common: Upper respiratory tract infection, headache, lymphopenia (b) Serious: Hepatotoxicity, infection, graft-vs.-host disease after transfusion iv. Contraindications: Current malignancy, women of reproductive potential, HIV infection, active chronic infections (e.g., hepatitis, tuberculosis), breastfeeding v. FDA boxed warning: Contraindicated for use in women and men of reproductive potential who do not plan to use effective contraception because of the potential for fetal harm. Advise females and males of reproductive potential to use effective contraception during cladribine treatment and for 6 months after treatment. vi. Drug interactions: Avoid immunosuppressive and antiviral/antiretroviral drugs, avoid live-attenuated vaccinations, hematotoxic drugs 3. Symptomatic therapies a. Patients may have fatigue, spasticity, urinary incontinence, pain, depression, cognitive impairment, fecal incontinence, constipation, pseudobulbar affect, and sexual dysfunction; standard therapies should be used for these symptoms. b. Fatigue: Treatment may be nonpharmacologic (rest, assistive devices, cooling strategies, exercise, stress management) or pharmacologic (amantadine, methylphenidate, modafinil, fluoxetine). c. Spasticity: Therapies must be centrally acting. i. First line: Baclofen, tizanidine ii. Second line: Dantrolene, diazepam iii. Third line: Intrathecal baclofen, gabapentin iv. Focal spasticity: Botulinum toxin d. Walking impairment: Dalfampridine (Ampyra) i. Indicated to improve walking in patients with MS by improving walking speed ii. Potassium channel blocker, prolongs action potentials in demyelinated neurons iii. Dose: 10 mg orally twice daily; extended-release tablets iv. Contraindicated in patients with a history of seizures or moderate or severe renal impairment v. Adverse effects: Seizures, UTIs, insomnia ACCP Updates in Therapeutics® 2023: The Pharmacotherapy Preparatory Review and Recertification Course 1-526 Neurology e. Pseudobulbar affect: Dextromethorphan/quinidine i. Affects 10% of patients ii. Episodes of inappropriate laughing or crying iii. Dextromethorphan prevents excitatory neurotransmitter release. iv. Low-dose quinidine blocks first-pass metabolism of dextromethorphan, thus increasing dextromethorphan serum concentrations. Table 9. Comparison of Disease-Modifying Therapies Generic (Brand) Alemtuzumab (Lemtrada) Cladribine (Mavenclad) Dimethyl fumarate (Tecfidera) Fingolimod (Gilenya) Dose First course: 12 mg/day over 4 hr × 5 days Second course: 12 mg/day over 4 hr × 3 days 12 mo after first course Recommended cumulative dose 3.5 mg/kg orally divided into 2 yearly courses. See labeling for detailed administration schedule 120 mg twice daily × 7 days; then 240 mg twice daily 0.5 mg Route IV Frequency Daily for 5 days; then daily for 3 days 12 mo later Adverse Effects Infusion reaction 92% Rash 53% Thyroid disorders 34% Headache 52% Infections 13%–19% PO Two cycles annually Upper respiratory tract infection (38%) Headache (25%) Lymphopenia (24%) PO Twice daily Skin flushing 38% GI events 41% PO Daily Increased AST/ALT 14% Infections 13% Diarrhea 12% Hypertension 6% Bradycardia 4% Blurred vision 4% Lymphopenia 4% Leukopenia 3% Glatiramer acetate (Copaxone) 20 mg 40 mg SC Daily Three times/wk Injection site reaction 90% Systemic reaction 15% Interferon beta-1a (Avonex) 30 mcg IM Weekly Flu-like symptoms 61% Anemia 8% Depression Interferon beta-1a (Rebif) 22 mcg or 44 mcg SC Three times/wk Flu-like symptoms 28% Injection site reactions 66% Leukopenia 22% Increased AST/ALT 17%–27% Depression Interferon beta-1b (Betaseron) 0.25 mg SC Every other day Flu-like symptoms 60%–76% Injection site reactions 50%–85% Asthenia 49% Menstrual disorder 17% Leukopenia 10%–16% Increased AST/ALT 4%–19% ACCP Updates in Therapeutics® 2023: The Pharmacotherapy Preparatory Review and Recertification Course 1-527 Neurology Table 9. Comparison of Disease-Modifying Therapies (Cont’d) Generic (Brand) Mitoxantrone (Novantrone) Dose 12 mg/m2 Up to 140 mg/m 2 (lifetime dose) Route IV Frequency Every 3 mo Natalizumab (Tysabri) 300 mg IV Every 4 wk Ocrelizumab (Ocrevus) Ofatumumab (Kesimpta) 300 mg, followed by 300 IV mg 2 wk later; then 600 mg SC Initial: 20 mg at week 0, 1, 2 Maintenance: 20 mg at week 4 and then monthly Pegylated interferon 125 mcg SC beta-1a (Plegridy) Adverse Effects Nausea 76% Alopecia 61% Menstrual disorders 61% UTI 32% Amenorrhea 25% Leukopenia 19% γ-Glutamyl transpeptidase increase of 15% Headache 38% Fatigue 27% Arthralgia 19% UTI 20% Hypersensitivity reaction < 1% Progressive multifocal leukoencephalopathy Every 6 mo after initial doses Weekly × 3 doses; then on week 4; then monthly Injection site reactions 34% Risk of infection Infection (52%) Injection site reactions (21%) Headache (13%) Every 2 wk Injection site reactions 62% Flu-like symptoms 47% Headache 44% Myalgia 19% Hepatic: Increased serum transaminases (23%); increased serum alanine aminotransferase (≥ 5 × upper limit of normal) 5%; ≥ 3 × upper limit of normal: 17%) Infection: 54%; serious or severe infection: ≤ 2% Respiratory: Upper respiratory tract infection (37%) Headache 15% Hypertension 13% Increased liver function tests 11% Falls 11% Peripheral edema 8% Nausea 7% Dizziness 7% Diarrhea 7% Bradycardia 6% Pain 6% Diarrhea 15%–18% Nausea 9%–14% Alopecia 10%–13% Neutropenia 10%–15% Lymphopenia 7%–10% Elevated ALT 3%–5% Hypertension 4% Peripheral neuropathy 1%–2% Reactivation of tuberculosis Ponesimod (Ponvory) PO Initial: Administer once daily according to a 14-day dose titration (in Table 8) Maintenance: 20 mg once daily, beginning on day 15 Once daily Siponimod (Mayzent) Depending on CYP2C9 genotype, usual dose titrate over 5 days to 1 mg PO Daily Teriflunomide (Aubagio) 7 mg or 14 mg PO Daily IM = intramuscular(ly); IV = intravenous(ly); PO = oral(ly); SC = subcutaneous(ly). ACCP Updates in Therapeutics® 2023: The Pharmacotherapy Preparatory Review and Recertification Course 1-528 Neurology B. Epidemiology 1. 30 million people in the United States have some form of peripheral neuropathy. 2. The most common form is diabetic neuropathy. Diabetic peripheral neuropathy can occur before an official diagnosis of diabetes and may be the presenting symptom of diabetes. C. Clinical Course 1.  Patients may initially present with altered sensation, pain, weakness, or autonomic symptoms. Symptoms typically are present distally in the initial stages. 2. Symptoms may be bilateral or unilateral, symmetrical, or asymmetrical. 3. Symptoms progress proximally. In advanced stages, distal wasting, weakness, absent deep tendon reflexes, and glove and stocking sensory loss can occur. D. Diagnosis 1. Complete medical history, medication history, and neurologic examination 2. Electromyelogram and nerve conduction studies 3. Laboratory tests to include serum chemistry, CBC, toxicology screen, vitamin B12 concentration, immune panel E. Causes Table 10. Common Causes of Acute Severe Peripheral Neuropathy Cause Guillain-Barré syndrome Vasculitis Diabetes Drugsa Porphyria Diphtheria Paraneoplastic neuropathy Acute idiopathic sensory neuropathy Critical illness Chronic inflammatory demyelinating polyneuropathy a Predominantly Motor + — — — + — — — + — Mixed + + + + — + + — + + Predominantly Sensory — — + + — — + + — — Examples include nitrofurantoin, vincristine, cisplatin, and reverse transcriptase inhibitors. F. Treatments 1. Most treatments are directed toward symptomatic relief of the sensory component of neuropathies. 2. Systemic and topical treatments may be combined. 3. If an immune component is involved, treatments include immune modulation. Recommendations for specific regimens vary with the disease diagnosis. a. Prednisone b. Immunoglobulin c. Plasmapheresis d. Immunosuppressants (e.g., cyclosporine, azathioprine, tacrolimus, sirolimus) ACCP Updates in Therapeutics® 2023: The Pharmacotherapy Preparatory Review and Recertification Course 1-530