Episodic/Paroxysmal disorders of the nervous system. DRUGS for headaches

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  1. Episodic/paroxysmal disorders
    general principles
    Discrete episodes - normal between

    Onset: sudden, progressive, insidious, provoked...


    • Step 1: characterize the episode
    • Step 2: what is the nature of the episode

    • -primary episodic disorder
    • -secondary to another category
  2. Headache and facial pain
    general principles
    • Pain sensitive structures:
    • -Cranial innervation for pain (CNV, high cervical spinal nerves)
    • -Most cranial structures

    • Insensitive structures
    • -Brain parenchyma
    • -much of the pia, arachnoid, and dura that covers the convexities of the brain
    • -Skull

    • Frequency of headaches
    • -*Migraine (45-50%)
    • -*Tension headache (45-50%)
    • -Cluster headache (1-2%)
    • -Brain tumor or other mass, subarachnoid hemorrhage, meningitis or other infection, other neurologic causes (<<1%)

    * "benign" primary headaches

    • Features that indicate significant underlying neurological disorder:
    • -Focal neurological signs or symptoms
    • -Recent or sudden onset of severe onset (new onset in older patients)
    • -Fever, stiff neck, lethargy or stupor
    • -Single persistent, worsening headaches
    • -worst headache of life (useless)
    • -Severe headache with onset during exertion
    • -Different in quality from pervious headaches
  3. Migraine
    ...wide variety of manifestations

    • Migraine w/o aura (common migraine)
    • -insidious onset
    • -builds to maximal intensity over 10-30 minutes
    • -lasts for several hours (rarely 24hrs)
    • -unilateral, pulsatile or throbbing, often located in the frontal region or behind the eye
    • -phonophobia, photophobia, nausea, and anorexia
    • -intensity can vary from mild, moderate, or severe

    • Migraine w/ aura (classic migraine)
    • -as above
    • -Focal neurologic symptomes and sometimes signs that are termed the aura
    • -Headache often occurs contralateral to the aura
    • Aura
    • - hallucination - sensory experience that is not due to external stimulation
    • --Visual scintillations and fortifications (most common)
    • --Paresthesias - tactile hallucination (next most common)
    • --Vertigo (rare)
    • ...very rare (dramatic) cases, the aura can be entirely negative, including hemiparesis, blindness, cognitive dysfunction such as aura
  4. Migraine
    epidemiology, Pathology, Pathophysiology
    • Epidemiology: very common... every age, every demographic
    • -Women > men (2:1)
    • -80% of patients have onset before the age of 30
    • -In women, often increased frequency during menses
    • -Strong familial component (but no mendelian pattern of inheritance has been shown)

    • Pathology: none
    • -rare cases, aura symptoms become permanent (path reveals ischemic stroke pattern without vascular disease)

    • Pathophysiology: many theories and specific observations
    • -Marching hypoperfusion - starting in the occipital lobes and marching forward during the aura; followed by rebound hyperperfusion phase (headache)
    • -Macrovascular dilation
    • -Spreading cortical depression (inhibition of electrical activity)
    • -Trigeminovascular (irritation of unmyelinated fibers of CNV)
    • -Serotoninergic
  5. Migraines
    evaluation and treatment
    Evaluation: history, rule out alternative pathologies (especially with worrisome auras - hemiparesis or aphasia - such as TIAs or epilepsy

    • Non-pharm: preventative lifestyle
    • -consistent sleep patterns, reduce caffeine, increase aerobic exercise
    • -avoid "triggers", but beware of incorrect associations

    • Pharmacologic treatment
    • Abortive treatment - to reduce the intensity and duration
    • -acetaminophen, aspirin, NSAIDs, have low efficacy for aborting. NOT a first line agent. Increased efficacy when combined with caffeine
    • -Compounnd analgesics + caffeine (narcotics, barbiturates, acetaminophen and NSAIDs) 40% are headache free two hours post tx. Rebound phenomena from overuse

    -Triptans (5-HT 1B/1D agonists) such as sumatriptan. Abort vascular cascade of inflammatory cytokines. Formulations include oral, intranasal, injectable (faster acting tend to have increased risk for side effects). Adverse effect: paresthesias, flushing, asthenia, fatigue, drowsiness, dizziness, nausea, sweating pressure in chest and neck, unpleasant taste. Peripheral vasoconstriction and vasospasm: contraindicated in patients with CAD, vascular disease. Some triptans are metabolized by MAO - should not be used by pts taking MAO inhibitors. Caution with patients taking SSRI or SNRI (serotonin syndrome)

    -Ergot alkaloids. generally less effective than triptans and have more side effects

    • Preventative treatment - reduce frequency and intensity of migraines
    • -pt with severe migraines, refractive to abortive therapy, frequency > 2x per week
    • -50-75% of patients have a 50% reduction in the headache frequency

    -Propranolol (non-selective beta blocker). Not a class effect. Contraindicated in pts with reactive airway disease

    -Divalproex (prolongs inactivation phase of voltage gated sodium channels, blocks T-type calcium channels) anticonvulsant/mood stabilizer. Not a class effect. Potent teratogen (neural tube defects)

    -Topiramate (prolongs inactivation phase of voltage gated sodium channels, potentiates GABA on GABAA receptor, blocks AMPA receptors). Adverse effects: metabolic acidosis, paresthesias, kidney stones, glaucoma, mental dullness. Dopamax. weight loss

    -Tricyclics (dirty SNRIs, plus variable anti-H1 antimuscarinic, and anti-alpha1 activity) Side effectsL anticholinergic effects (sedation, dry mouth, constipation, urinary retension)

    -NSAIDs (ibuprofen)

    • -Recent studies indicate that ACE inhibitors can reduce frequency and severity of migraine
    • -Botulinum toxin can reduce the frequency of migraine. Efficacy: (poor) reduces from 15 days/month to 10 days/month
  6. Tension headache
    presentation, pathology, pathophysiology
    • Clinical: insidious onset, slow evolution over hours 
    • -resolution over hours to days (only one that can last for days)
    • -frequency and severity tends to decrease over the years
    • -Pain: dull tightness or pressure, in a band-like distribution around the head and often down the neck and shoulders
    • -rarely acutely disruptive
    • -no other neurological symptoms (auras)

    • Epidemiology: most common type of headache, lifetime prevalence of essentially 100%
    • -Women > men
    • -Onset typically after 3rd decade of life. middle age
    • -overrepresentation of tension headaches correlating with physical or emotional stress

    Pathology: none

    • Pathophysiology: unclear
    • -debate about muscles of scalp and neck are actually tense during headaches, causative or reactive to pain (?)
  7. Tension Headaches
    evaluation and treatment
    Evaluation: characterize episodes, exclude alternative possibilities (temporal arteritis, lesion, "medication overuse headaches")

    Abortive treatment: over the counter analgesics, compound analgesics

    • Preventative therapy: use if frequency of >twice per week
    • -less evidence based than migraines
    • -Tricyclics
    • -relaxation, biofeedback, meditation, massage, exercise
  8. Cluster headaches
    • Clinical: Extremely severe stabbing or boring quality (non-throbbing pain)
    • -located behind, in and/or around one eye
    • -onset over minutes; duration in the range of 30-90 minutes
    • -Pts sometimes get ipsilateral Horner's syndrome (ptosis, miosis, anhidrosis), as well as lacrimation and nasal congestion or rhinorrhea

    • -Cluster: tendency for headaches to cluster in time (typically one or more times each day for weeks or months)
    • -more commonly at night
    • -alcohol will precipitate a typical headache

    • Epidemiology: uncommon disorder
    • -Male > female (5-10:1)
    • -Onset ranges from 20 to 50 years of age

    • Patho/Pathophys: no known/unclear
    • -Carotid artery swells during headaches, which could distort sympathetic plexus (lead to Horner's syndrome)

    Evaluation: characteristic history often makes differential dx limited. Temporal arteritis can be excluded with a normal ESR

    • Abortive treatment: 
    • -100% O2 by facemask for 10-15 minutes
    • -intranasal lidocaine
    • -intranasal or subcutaneous triptans typically abort attacks

    • Prevention of clusters:
    • -daily meds: verapamil, lithium, topiramate
  9. Epilepsy due to medial temporal sclerosis
    Epileptic pts whose seizure focus is located in the medial portion of one of their temporal lobes

    : paroxysmal interruption of normal cerebral electrical activity associated with a behavioral or cognitive change

    -Epilepsy: susceptibility to recurrent unprovoked seizures

    -Aura: subjective symptoms due to the first part of the seizures; not all seizures are preceded by an aura

    • Localize to temporal lobe:
    • 1. certain hallucinations (smell of burning tires, taste of copper, sight of familiar image or an illusion),
    • -illusions (such as enlargement or shrinking of particular objects),
    • -cognitive changes (sensation of deja vu, jamais vu, depersonlaization, emotional discordance)

    2. Alteration (but not complete loss) of consciousness. [focal seizure + altered level of consciousness (but not complete loss) = partial complex] Usually temporal, but sometimes frontal lobe.

    3. Simple motor behavior (automatism like lip-smacking, chewing, swallowing, grasping, patting movements) or more complex movements (walking, running, laughing) that occur during the time the pt has an abnormal level of consciousness

    • Epidemiology: any point in life
    • -usual cuases: trauma, stroke, infection (not discussed here)

    • Pts that don't have these causes...
    • -Onset: adolescence
    • -often have seizures that become secondarily generalized
    • -often respond well to medical therapy

    • Pathology: medial aspect of the temporal lobe is shunken and hardened (medial temporal sclerosis)
    • -Micro: non-specific neuron loss and gliosis

    • Pathophysiology: not clear
    • -perinatal brain injury to the medial temporal lobe; gliotic scar from perinatal injury serves as the seizure focus

    • Evaluation: history of partial complex seizures with onset in adolescence
    • -MRI: small hippocampal formation
    • -EEG shows interictal epileptiform discharges arising in the medial temporal lobe
    • -diagnostic trial with epileptic drug

    Treatment: pharmacologic is cornerstone; but surgical management can be important

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  10. Childhood absence epilepsy
    • Mostly in children, involves transient behavioral arrest with a blank stare that lasts a few seconds
    • -may have mild motor movements (blinking)

    aka petit mal

    • Onset: after the age of 4
    • -child may have innumerable episodes in a day
    • -attacks diminish in frequency in adolescence; almost always resolve
    • -50% will also have generalized tonic clonic seizures

    Strong genetic component (85% concordance in twin studies)

    Pathology: none

    • Pathophysiology: not known
    • -EEG shows synchronous diffuse 3 Hz spike and wave discharges during their absences
    • -Presumed thalamic involvement

    • Evaluation: clinical suspicion
    • -can be provoked by hyperventilation

    • Treatment: anticonvulsant therapy
    • -most spontaneously resolve
    • -children who continue to have seizures typically begin to have generalized tonic clonic seizures

    • Rx: ethosuximide and divalproex (block T-type calcium channels)
    • -Ethosuximide - well tolerated, treats absence seizures, but no other type of seizure including generalized tonic clonic seizures that develop in about half of patients with childhood absence epilepsy
    • -Divalproex - effective for absence and other types of epilepsy. Can be hepatotoxic; not for children <5 years old
  11. Syncope and presyncope
    • Episode of loss of consciousness associated with loss of postural tone
    • -due to global hypoperfusion of the cerebral hemispheres or the brain stem

    Presyncope: variable prodrome that often accompanies the onset of hypoperfusion. Sense of queasiness, pallor, clamminess, confusion, graying of vision and ringing in ears

    Clinical: flaccidly collapse to the ground. May have brief twitching movements or eye rolling behavior

    • Etiology:
    • 1. Decreased CO - outflow obstruction, bradyarrhythmias, non-perfusing tachyarrhythmias

    • 2. Vasovagal (common faint): decrease in sympathetic vascular tone with an increase in vagal tone leading to bradycardia and hypotension
    • -emotional stimuli
    • -(no pathology)

    • 3. Orthostatic hypotension: BP drops upon standing
    • -hypovolemia
    • -dysautonomia - lack of compensatory changes

    • Evaluation: cardiac monitoring/work-up
    • -EMG and nerve conduction studies
    • -Tilt-table testing

    Treatment: most is vasovagal; tx is to avoid precipitating events, education
  12. Transient global amnesia
    • sudden onset of an isolated "basic amnesia syndrome"
    • -anterograde amnesia for both verbal and non-verbal material
    • -retrograde amnesia
    • -normal immediate memory
    • -normal procedural memory

    Resolves within 24 hrs

    • Presentation: pts often draw attention because they have no recall, repeat questions
    • -typical onset is in middle age
    • -recurrence rate is about 4-5% per year

    Pathophysiology: thought to be due to chemically mediated local hypoperfusion (akin to what is seen in migraine with aura). Dysfunction never progresses to infarction
  13. Drugs for headache
    • Tension headaches:
    • -NSAIDs (acetaminophen, ibuprofen)

    • Migraine
    • Acute
    • -NSAIDS (acetaminophen, ibuprofen)
    • -Triptans (sumatriptan [Imitrex])
    • -Ergot alkaloids (ergotamine, not as effective as triptans)
    • Prevention
    • -Propranolol
    • -Verapamil (L-type calcium channel blocker)
    • -Tricyclic antidepressant - TCA (Amitriptyline, Desipramine Nortriptyline) 
    • -Divalproex (prolong inactivated state of Na+ channels and block T-type Ca channels)
    • -Topiramate (prolong inactivated state of Na+ channels and block T-type Ca channels)
    • -NSAIDs (acetaminophen, ibuprofen)
    • -Botulinum toxin

    • Cluster headaches
    • Acute
    • -Oxygen
    • -Triptans (Sumitriptan)
    • Prevention
    • -Verapamil (inhibits L-type Ca channels)
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Episodic/Paroxysmal disorders of the nervous system. DRUGS for headaches
2013-02-01 01:53:44

Episodic and paroxysmal disorders. Drugs for headaches
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