Neuromuscular

• Medications for Parkinson's Disease

  • Levodopa
  • Levodopa/Carbidopa (Sinemet)
  • Pramipexole (Mirapex)
  • Selegiline (Deprenyl)
  • Anticholinergics
• Levodopa Mechanism of Action

  Levodopa enters the brain (crosses the BBB) and converts to dopamine, thus restoring a balance between acetylcholine and dopamine
• Levodopa does not cure PD or delay disease progression
• Levodopa

  • Administered orally, therapeutic response can take several months
  • Most effective drug for PD
• Effectiveness of Levodopa decreases over time (symptoms are usually well controlled in first 2 years of treatment and effectiveness declines)
• Carbidopa


  Has no therapeutic effects on its own, delays the process of peripheral drug metabolism, allowing for more levodopa to enter the brain
• Patients on sinemet should avoid high protein meals BECAUSE they compete for absorption in gut
• On/Off Phenomenon

  1. Abrupt/acute return of PD symptoms

  2. On Phenomenon = therapeutic effect & reduction of symptoms

  3. Off Phenomenon = sudden return of PD symptoms (lasting minutes – hours) / Increased intensity & frequency with time
• Wearing off phenomenon

  1. Gradual return of PD symptoms

  2. Related to gradual loss of effect of Levodopa; return of symptoms are generally seen at the end of a dose interval when drug levels are low
• Pramipexole (Mirapex)

  Non-ergot dopamine receptor agonist, stimulates dopamine receptors in the striatum
• Pramipexole (Mirapex) does not cure PD or delay progression of disease
• Pramipexole (Mirapex)

  • Stimulates parts of the brain that need dopamine
  • Less likely to cause disabling dyskinesias
  • Improves motor symptoms
  • Not dependent on enzymatic conversion, not converting to toxic metabolites, does not compete with dietary proteins for uptake in the intestine, or transport across the BBB
• Selegiline (Deprenyl)

  MAO-B Inhibitor, suppresses the destruction of dopamine derived from Levodopa which prolongs the effects of Levodopa and decreases consequential fluctuations in motor control – thereby reducing on-off & wearing off effect
• Anticholinergics

  Block action of acetylcholine, often used in combination with other antiparkinsonian medications
• In Parkinson's there is an imbalance between dopamine and acetylcholine
• Methylprednisolone (Solu-Medrol)

  Mimics cortisol (a hormone produced by our adrenal glands) + potent anti-inflammatory and immunosuppressant. Works rapidly and is often only used for a short period of time
• Anticholinergics

  Indication: Parkinson's, asthma, COPD, incontinence, dizziness, diarrhea
• Anticholinergics


  • Studies show it can greatly improve tremors, does not improve bradykinesia + used in younger patients with mild symptoms
• Anticholinergics

  Common side effects include blurred vision, dry mouth, constipation, and urinary retention + In the elderly, there is increased risk of cognitive decline developing dementia and confusion not prescribed to patients above the age of 70. DO NOT GIVE OVER THE AGE OF 70!
• Methylprednisolone (Solu-Medrol)


  • Anti-inflammatory and immunosuppressive effects + helps protect nerves
• Methylprednisolone


  Available as IV and IM + Monitor closely for signs of acute infection (fever, increased WBC, cough, soft tissue pain/swelling, UTI symptoms) + Solumedrol given IV + predni. Given oral
• Glucocorticoids are immunosuppressive and can exacerbate infections
• Interferon Beta Drugs (Betaseron)

  Naturally occurring glycoprotein + Inhibits migration of proinflammatory leukocytes across the blood brain barrier (cannot reach neurons of the CNS)
• Interferon Beta Drugs (Betaseron)


  • Suppresses t-helper cell activity
• Interferon Beta Drugs (Betaseron)

  • Can decrease the frequency and severity of relapse, reduce the size and number of lesions, and delay progression of disability
• Interferon Beta Drugs (Betaseron)

  Intramuscular or Subcutaneous + depends on the specific drug + Given ASAP after diagnosis (early treatment prevents degen.)
• Interferon Beta Drugs (Betaseron) reduces development of brain lesions, and may prevent perman. Damage to axons. + can be used long-term
• Interferon Beta Drugs (Betaseron)


  Stop pro inflamm. leukocytes from reaching BBB, and saves the myelin of the neuron, and supp. T helper cell activity, suppressing the immu. Response.
• Interferon Beta Drugs (Betaseron)

  • Flu-like symptoms such as headache, fever, chills, malaise, muscle aches, and stiffness
• Interferon Beta Drugs (Betaseron)


  • Causes myelosuppression (can suppress bone marrow function, decreasing production of all blood cells)
• Interferon Beta Drugs (Betaseron)

  • Causes depression and suicidal ideation
• Mitoxantrone (Novantrone)

  Immunosuppressant + Cytotoxic drug. This means it kills cells in the body. Used to be a cancer drug!
• Mitoxantrone (Novantrone)

  It binds with DNA and inhibits DNA and RNA synthesis, causing breakage of DNA strands.
• Like chemotherapy, Mitoxantrone is more lethal to cells that divide fast - hair, skin, GI mucosa, and bone marrow
• Mitoxantrone (Novantrone)

  • Suppresses production of immune system cells and decreases immune system destruction of myelin
• Mitoxantrone (Novantrone)


  • It can delay MS patients going into relapse, delays disability progression, and can decrease lesions
• Mitoxantrone (Novantrone)

  • Myelosuppression = toxic to bone marrow cells causing decreased platelets, white blood cells, and red blood cells. Reduced neutrophils leads to high risk of infection
• Mitoxantrone (Novantrone)

  • Cardiotoxicity = affects the left ventricular ejection fraction and can cause heart failure. This can occur months to years after treatment has ended
• Mitoxantrone (Novantrone)

  • Teratogenic = potential for fetal harm
• Mitoxantrone (Novantrone)

  • Causes hair loss, nausea/vomiting, and mouth sores + all related to the death of rapidly dividing cells