Chronic Neurological Diseases

•Pain sensitive structures in head:

–The dura mater

–The arteries in the meninges.

–Larger cerebral arteries.

–Sinuses.

–Cranial Nerves V, IX, X.

–Upper cervical nerves.

–Head and neck muscles.

•Not necessarily muscle tension.

•Neurovascular factors.

•Usually bilateral.

•Mild to moderate severity.

•Worse with exertion.

•+/- photophobia/phonophobia.

•Treatment with NSAID, ASA or Acetaminophen.

•Throbbing, usually unilateral.

•Female predominance.

•Family history.

•Pathophysiology: serotonin mediated cerebrovascular dilation and stimulation of pain fibers.

•Moderate to severe and disabling.

•Can last hours to days.

•Associated triggers.

• 1.Triggers include
• menses, ETOH, stress, foods.

• 2.Patient wants to be
• in quiet dark room.

•Aura

•Unilateral or bilateral.

•Severe photophobia and phonophobia.

•Nausea and vomiting.

Precedes in 10 %. Flashing lights, weakness, numbness, field defects.

Abortive Therapy:

• –Triptans
• e.g. sumitriptan (Imitrex®)

• –Ergotamine:
• DHE

•Prophylaxis:

• –Βeta
• Blockers

–Calcium Channel Blockers

• –Tricyclic
• Antidepressants

–Anticonvulsants


•Identify Triggers

• 1.Available in pill, injection, nasal spray. Can cause vasoconstriction (Contraindicated in CAD).
• 2.Premedicate for nausea. Causes vasoconstriction.
• 3.Red wine, cheese,
• MSG, caffeine, fermented food, aspartame, chocolate.

•Occur in clusters for weeks to months.

•Male predominance.

•Vasodilation in trigeminal area.

•Severe stabbing orbital, supraorbital or temporal pain.

•Sudden onset.

•Lasts 30-90 minutes.

• •Associated with tearing, miosis,
• ptosis, conjunctival injection.

Patient paces is restless.

•High flow O2.

•Ergotamine.

•Prophylaxis: Calcium Channel Blockers (Verapamil).

•Temporal Arteritis.

•Trigeminal Neuralgia.

•Tumor.

•Aneurysm.

•Infection.

Trauma

1.ESR. Temporal artery biopsy.

2.Severe lacinating pain triggered by touch.

•None indicated if diagnosis is clear.

•CT or MRI for trauma, focal deficits.

•LP for suspected infection.

•Autoimmune degeneration of CNS.

•Demyelination.

•Gliosis

•More common in Europeans.

•Family history.

•Possible viral trigger.

•Variable symptoms and course.

• Relapsing Remitting
• Clearly defined relapses with full or partial recovery.
• Primary Progressive
• Disease progressive from onset.
• Secondary Progressive
• Begins as relapsing-remitting then becomes progressive.
• Progressive Relapsing
• Progressive disease with periods of acute exacerbation progression

•Highly Variable.

•Weakness.

•Diplopia.

•Muscle Spacticity.

•Numbness and Tingling.

•Bladder Symptoms.

•Neuropathic Pain.

•Ataxia.

•Dysarthria

•Dysphagia

Lhermitte’s Phenomenon.

•Clinical Evaluation.

•MRI.

•Corticosteroids.

–For acute exacerbations.

–Do not change long-term prognosis

–Taper Dosage.

–Multiple Side Effects.

•Beta-interferon.

• –Decreased
• Exacerbation.

Self-injection.

1.Give with food. Risk of hyperglycemia, PUD, fluid retention, osteoporosis, psychosis, depression, poor wound healing.

• 2.Flu like symptoms, skin reactions, depression.
• Monitor CBC, LFTs.

•Bethanechol for Flaccid Bladder.

–Cholinergic.

• •Oxybutynin
• (Ditropan®)
• or Tolterodine (Detrol®)
• for Bladder Spasms.

–Anticholinergic.

•Baclofen for muscle spasms.

–Sedation.

Decrease in seizure threshold

•Infections.

•Post-partum.

•Stress.

•Head Trauma.

•Climate Change.

•Neuro Assessment.

•Psychosocial Assessment.

•Pain Assessment.

•Management of Immobility.

•Management of Elimination.

•Management of Safety.

•Patient Education.

•Arrange Home Care, PT/OT/Speech

• 1.Establish baseline.
• 2.Coping, social resources, family relationships.
• 3.Neuropathic, spastic. Medications, positioning, massage etc.
• 4.Skin, Pulmonary, DVT risk.
• 5.Bladder, Constipation. High risk of UTI,
• impaction. May need I+O cath or disimpaction.
• 6.Fall risk. Aspiration risk.
• Medications, Adequate rest, Avoidance of stress, infection.

•Disease of Basal Ganglia.

•Degeneration of substantia nigra.

•Imbalance of dopamine and acetylcholine.

•Incidence increases with age.

•♂ greater than ♀ 3:2.

•Usually Idiopathic.

• •Can be triggered by neurotoxins or
• medications.

•Insidious Onset.

•Tremor.

•Bradykinesia.

•Rigidity.

•Loss of postural reflexes.

• •Clinical diagnosis
• 1.Slowly progressive.
• 2.Pill rolling, Resting.
• 3.Difficulty initiating movement.
• 4.Stiffness, cog-wheel.
• 5.No diagnostic test.

•Masked facies.

•Drooling.

•Loss of arm swing.

•Shuffling gait.

•Dysphagia.

•Hypophonia.

•

•Aspiration.

•Depression.

•Falls.

•Dementia.

Complications of Immobility

•Levodopa/Carbidopa (Sinemet®).

• •Dopamine Agonists: Ropinirole (Requip®), Pramipexole
• (Mirapex®), rotigotine (Neupro®)

•Entacapone (Comtan®)

• •Anticholinergic:
• Benztropine
• (Cogentin®)

•Stalevo®

• 1.L-dopa crosses BB
• barrier. C dopa prevents enzyme
• breakdown in periphery.
• Orthostatic hypotension, psychosis, N/V, dyskinesias, looses
• effectiveness.

• 2.Stimulates dopamine
• receptors. Edema, sedation, N/V,
• orthostatic hypotension, psychosis, compulsive behavior.

• 3.Blocks COMT
• enzyme. Decreases breakdown of L-Dopa.

• 4.Primarily for
• tremor. Anticholinergic side effects.

5.Combination of Sinemet and Comtan.

•PT/OT/Speech

•Diet Issues

–Protein

•Deep Brain Stimulation (DBS)

• –Generator
• placed in chest

–Adjustable

–Reversible

•Protect from injury.

•Promote mobility.

•Prevent aspiration.

• •Assess for therapeutic or adverse effects of
• medications.

•Timing of medication.

•Patient education.

•“Grave Weakness”

•Autoimmune disease of neuromuscular junction.

•Worsens with exertion improves with rest.

• •Affects eye movements, chewing, swallowing,
• speaking, breathing.

• •Exacerbations triggered by stress, menses,
• pregnancy, trauma, infection, illness, medications, temperature extremes.

Antibodies attack Ach receptors

•Aminoglycosides.

•Procainamide.

•Beta Blockers.

•Quinidine.

•Phenytoin.

•Neuromuscular Blockers.

•Acetylcholine receptor antibodies.

• –85-90
• % of patients.

•Electromyelogram (EMG)

• –Decreased
• muscle response with repetition.

• •Tensilon
• test.

• –Short
• acting acetylcholinesterase blocker Endrophonium
• (Tensilon®).

–Improvement indicates MG.

–Atropine on hand

•Neostigmine (Prostigmine®) an anticholinesterase inhibitor.

•Corticosteroids.

•Immunosuppressants Azathioprine (Imuran®).

•Thymectomy


•Plasmaphoresis.

•Myasthenic Crisis: Severe exacerbation of muscle weakness.

–Impacts swallowing and breathing.

• •Cholinergic Crisis: Similar
• presentation. Caused by excessive Neostigmin or other cholinergic drugs.

•Differentiate with Tensilon Test.

•Assess Respiratory Status.

•Assess Swallowing.

• •Schedule Neostigmine to coincide with meals
• or periods of activity.

•Plan frequent rest periods.

•Patient Education.

•Psychosocial Support.

• •Degeneration of motor neurons in brain and
• spinal cord.

•Onset age 40-70. ♂ >♀ 2:1.

• •Progressive weakness, dysarthria, dysphagia,
• respiratory failure.

•Need for advanced directives.

•

•Autosomal dominant inheritance.

•Higher incidence in Europeans.

•Onset age 30-50.

• •Deficit of Acetylcholine and GABA leads to
• excessive Dopamine.

• •Causes chorea, ataxia, psychosis and
• dementia.

• •Treatment is symptomatic: Haldol,
• SSRIs, Clonazepam (Klonopin®)

•Genetic Testing.

Answer Unknown

• –A)
• Her symptoms will improve with Neostigmine (Prostigmine®)

• –B) A Tensilon test will be needed to establish the
• etiology of the crisis.

• –C) Acetylcholine Receptor antibodies will be
• decreased.

–D) None of the above.

Answer Unknown

• –A)
• Review his medication dosage and scheduling, and discuss with the physician.

• –B)
• Encourage him to nap when this happens.

• –C)
• Tell him to increase the duration of his morning walk to strengthen his
• muscles.

• –D)
• All of the above.