Pain

Comments

Acute vs chronic pain • Acute pain: < 3 months

• Chronic pain: ≥ 3 months
1. Reduced pain thresholds
2. Central behavioral changes
3. Refractory to acute pain therapy

Allodynia Pain caused by a stimulus that does not normally cause pain

Analgesia Absence of pain in response to normally painful stimuli

Anesthesia dolorosa Pain in an area or region that is anesthetic

Heterotopic pain Pain source not located in region of pain perception but within same dermatome

Hyperalgesia An increased pain response (more pain) to a normally painful stimulus

Hypoalgesia Diminished pain in response to a normally painful stimulus

Hypoesthesia Decreased sensitivity to sensory stimulation (excludes the special senses)

Paresthesia An abnormal sensation, whether spontaneous or evoked

Referred pain Pain felt at a location innervated by 1 nerve, but nociceptive impulses arrive on a
different nerve  (can be from a different dermatome)

Sensitization • An increase in excitability of neurons

• 2 mechanisms 1- Peripheral
º A reduction in threshold and an increase in responsiveness of peripheral ends of
nociceptors Example: Pain after sunburn
º Sensitization arises due to action of inflammatory chemicals
2-Central
º Increase in excitability of neurons within central nervous system so that normal
inputs begin to produce abnormal responses º Example: Tactile allodynia

Neuropathic Pain Disorders

Episodic

1. Severe, paroxysmal electric shock−like and/or lancinating pain

2. short duration

Continuous

1. Aching
2. Burning
3. Throbbing, Stabbing Pain

Quantitative sensory testing

– Heat activates  C-fibers

1. Unmyelinated
2. Small-Diameter
3. Slow Conduction

– Cold stimuli and punctate mechanical stimuli activate  A-delta fibers

1. Myelinated
2. Large-Diameter
3. Fast Conduction
4. Afferent Fibers Only

– Electrical stimuli activate  A-beta fibers

1. Myelinated
2. Large-Diameter
3. Fast Conduction
4. Both Afferent And Efferent Fibers
Episodic neuropathic pain Continuous neuropathic pain

1. Trigeminal neuralgia 1. Idiopathic trigeminal neuropathic

2. Glossopharyngeal neuralgia pain
2. Post-herpetic neuralgia
3. Central post-stroke pain
4. Complex regional pain syndrome
(CRPS)
Episodic Neuropathic Pain Disorders
Trigeminal neuralgia (TN)
Pathophysiology
– Most common hypothesis

Vascular compression of trigeminal nerve root entry zone  demyelination

spontaneous nerve firing

Signs and symptoms:

1. Excruciating
2. short-lasting
3. shock-like facial pain
4. Unilateral,
5. R > L– V2 and V3 > V1
6. No neurologic deficits–
7. Frequently pain free between attacks
8. Local anesthesia of trigger point temporarily arrests pain

Trigger points  Areas in distribution of affected trigeminal branch

(lip, nose, eye, inside mouth) initiate pain when touched
Types
1. Classic TN  85% of cases
2. Atypical TN  Longer attacks and constant background pain
3. Symptomatic TN  Various forms of etiologic pathology including
tumors, vascular malformations
Episodic Neuropathic Pain Disorders

Trigeminal neuralgia (TN)

Differential diagnosis

1. Multiple sclerosis
2. Intracranial tumor : Posterior and middle fossa

Treatment

Pharmacology

1st line: Carbamazepine

2nd line: Phenytoin– Surgery

Peripheral procedure

– Neurectomy Cryotherapy Alcohol injection

Central procedure

1. Percutaneous rhizotomy
2. Microvascular decompression
3. Gamma Knife radiosurg
Episodic Neuropathic Pain Disorders
Glossopharyngeal neuralgia (GN)
Pharyngeal GN
1. Pain in pharynx, tonsil, soft palate, posterior tongue base
2. Pain radiates toward mandibular angle
Tympanic GN
– Pain in ear
– Pain may radiate to pharynx (can be confused with geniculate neuralgia)
• Pain triggered by  swallowing, chewing, talking, coughing, yawning
• Can induce  bradycardia and syncope
• Order (MRI)  rule out pathology (symptomatic GN)
1. Tonsillar carcinoma in parapharyngeal space
2. cerebellopontine angle mass
3. vascular anomalies

Medical treatment  Similar to TN

1. Intracranial cranial nerve 9

2. X upper rootlet sectioning
3. Microvascular decompression
Continuous Neuropathic Pain Disorders

Idiopathic trigeminal neuropathic pain

 Chronic dental or facial pain that does not meet any diagnostic criteria
And Does Not Respond To Most Treatments,
 Females > Males,
 Maxilla > Mandible

• Symptoms

1. Dull aching or throbbing pain,

2. Paresthesia
3. Present continuously for months or years with intermittent periods of
increased pain

• Subtypes

Atypical odontalgia/phantom tooth pain

Pain confined to teeth and gingival area

Atypical facial pain

Pain involves parts of the face

Treatment

Tricyclic antidepressants, gabapentin, pregabalin, tramadol, topical

lidocaine
Continuous Neuropathic Pain Disorders

Post herpetic neuralgia

Reactivation of latent infection  varicella zoster virus dormant in

peripheral ganglion

• 16% to 22% of patients experience

1. Neuralgia
2. Burning
3. Throbbing
4. shooting or sharp pain;

May be accompanied by
1. Allodynia
2. Hyperalgesia
3. Anesthesia Dolorosa

•Associated with pale or reddish scars  Hypoesthetic or Anesthetic

– V1 distribution (80%)  if cranial nerve 5 affected

– Ramsay Hunt syndrome Herpes zoster infection of sensory and motor

branches of cranial nerve 7 +/- cranial nerve 8

Associated with facial paralysis Vertigo, Deafness, Anesthesia Dolorosa

Treatment
1. Tricyclic antidepressants
2. Gabapentin & pregabalin
3. Opioids & tramadol
4. Topical lidocaine
Continuous Neuropathic Pain Disorders

Central post stroke pain

• Develops in approximately 8% of post-stroke patients
• After a stroke brain does not understand normal messages sent from
body in response to touch, warmth, cold, and other stimuli
Signs
1. Pain
2. Dysesthesia
3. impaired sensation to pinprick and temperature stimulation
4. slight sensation may be painful

• Pain may be
1. Constant or episodic
2. Onset may be more than a month after stroke

Treatment

 1st line
1. Amitriptyline
2. lamotrigine
 2nd line
1. Mexiletine
2. Phenytoin
3. Intravenous ketamine
4. propofol
5. lidocaine
Continuous Neuropathic Pain Disorders

CRPS
- Severe pain, swelling, and skin changes associated with history of nerve
and tissue injury & sympathetic symptoms (ex lacrimation)
- Worsens over time
- Associated with dysregulation of central nervous system and autonomic
nervous system

Sympathetic nervous system:

1. Edema
2. Cutaneous Blood Flow Changes
3. Motor Changes
4. Trophic Changes

Often termed Hot or cold CRPS based on skin temperature of affected area

- Hot CRPSAcute condition

- Cold CRPS  Chronic condition( poorer prognosis )

2 Types

Type 1 (reflex sympathetic dystrophy)

1. Presence of a noxious initiating event without nerve damage

2. Aching, pricking, burning pain

Type 2 (causalgia)

1. Presence of a noxious initiating event with nerve damage

2. Electric and/or shooting pain
Continuous Neuropathic Pain Disorders

CRPS
Treatment
1. Physical therapy and/or occupational therapy
2. Tricyclic Antidepressants
3. Selective Serotonin Reuptake Inhibitors
4. Anticonvulsants
5. Gabapentin
6. Steroids
7. Opioids
8. Local anesthetic injections
9. Neurostimulation
10.Sympathectomy
11.Awake and/or subanesthetic low-dose intravenous ketamine infusion

Headache

Primary headaches

1. Migraine
2. Tension-type headache
3. Cluster headache
4. Paroxysmal hemicrania

Secondary headaches

1. Temporal arteritis 2. Posttraumatic headache

Primary Headache Disorders
• Primary VS secondary headache
– Primary headache No other cause
– Secondary headache  In close temporal relation to another disorder

Migraine headache
• Commonly starts at age 15–24, but most frequent at ages 35–45

females > males

4 Possible Phases:

1. Predromal
2. Aura
3. Pain
4. Postdromal

Pathophysiology  Neurovascular disorder

Symptoms

1. Unilateral pulsing headache lasting 2–72 hours

2. Associated with nausea, vomiting
3. Sensitivity to light, sound, and smell

Types

1. Common migraine without aura

2. Classic migraine with aura
3. Chronic migraine: 15 days per month
4. Status migranosus: Lasts > 3 days
Migraine headache

Treatment

- Symptomatic

Specific

5-hydroxytryptamine (5-HT) agonists (triptans), dihydroergotamine

Nonspecific:

1. Acetaminophen
2. acetylsalicylic acid (ASA),
3. (NSAIDs), caffeine

- Prophylactic

Most effective

1. Tricyclic Antidepressants
2. Sodium Valproate
3. Topramate, Timodol

Moderately effective:

1. Gabapentin
2. Verapamil
3. Naproxen
Tension Headache

 Onset  20 – 40 years
 Female More

Pathophysiology

– Triggers  Stress, hunger, sleep deprivation, bad posture, eye strain

– Classic theory  Muscle contraction/tension

Symptoms:

Bilateral pressing/tightening

(nonpulsatile) quality

Treatment

– Episodic type  NSAIDs, acetaminophen, ASA;

Frequent use of these drugs  lead to rebound headache

– Chronic type  Amitriptyline, mirtazapine, relaxation techniques

Paroxysmal hemicrania

Sjaastad Syndrome

Similar to cluster headache but

1. Shorter duration  2–30 minutes

2. More frequent
3. More common in females
4. 100% responsive to indomethacin
Cluster headache
• Onset  27–31 years
• Males > females
Pathophysiology:
Hypothalamic abnormality
Symptoms
1. Severe unilateral orbital
2. Supraorbital, temporal pain  lasting 15–180 minutes
3. Accompanied by  ipsilateral lacrimation
4. Rhinorrhea
5. Eyelid Edema
6. Miosis1 to 8 attacks per day

Symptomatic/abortive

1. Oxygen (7 L per minute for 15 minutes)

2. triptans, dihydroergotamine

Prophylactic

1. Verapamil (1st line)

2. Short-Term Corticosteroid
3. Lithium
4. Divalproex Sodium
5. Topiramate
Intractable type Invasive Procedure

1. Sphenopalatine block
2. Microvascular Decompression of trigeminal nerve
Secondary headaches
Temporal arteritis
• Vasculitis of large and medium arteries of head, predominately external
carotid artery branches (frequently temporal artery)
• May rapidly lead to blindness  due to giant-cell granulomatous
occlusion of ophthalmic artery
• Suspect if 
1- Patient > 50 years
2- New persistent headache centered on 1 or both temples
3- Worsened by cold temperatures, associated with jaw claudication
Diagnosis
1. Prominent temporal artery
2. Temporal tenderness
3. Decreased temporal pulse
4. Ischemic fundus
5. Increased ESR and C-reactive protein
6. Biopsy (gold standard) Unilateral temporal artery biopsy of 1.5 to 3 cm
has 85% to 90% sensitivity
Treatment
Corticosteroid as soon as possible before diagnosis confirmed by biopsy
Why ?
Prevent permanent blindness due to ophthalmic artery occlusion
Secondary headaches
Posttraumatic headache
1. Post–closed-head injury syndrome
2. Post concussion syndrome

Diagnostic criteria
1. Head trauma with persistent posttraumatic amnesia
2. loss of consciousness or posttraumatic seizure + neuropsychologic
impairment + 3 of following for > 3 months postinjury changes
1. Headache, dizziness, fatigue
2. Irritability, sleep problems
3. Afect changes
4. Personality
Treatment
1- Eliminate aggravating extracranial nociceptive pain sources
2- Neuropsychiatric disability rehabilitation
3- Tricyclic antidepressants, gabapentin, pregabalin