P A I Nfocus on
LBP and HEADACHE
Department Of Neurology
dr. Hasan Sadikin Hospital Padjadjaran University
Definition of PAIN
Pain is unpleasent sensory and emotional experience associated with actual or potential tissue damage, or discribed in term of such damage ( IASP, 1986 )
Pain Clinical Diagnosis
• History taking
• Physical examination, Neurological exam.
• Laboratory examination :
Lab.
Neurophysiology exam.
Neuroimaging
Visual Analog ScalesVisual Analog Scales
00 1010
NoNopainpain
ExcruciatingExcruciatingpainpain
00 1010
CompleteCompletepain reliefpain relief
NoNopain reliefpain relief
McQuay, 1998.Note: Lines must be exactly 100 mm long
FACES SCALES
LOW BACK PAIN(NYERI PUNGGUNG BAWAH)
• Nyeri di antara sudut iga terbawah dan lipat bokong bawah yaitu di daerah lumbal atau lumbo-sakral dan sering disertai dengan penjalaran nyeri kearah tungkai-kaki
Pain sensitive L-S structures
• Skin, subcutaneous, adipose tissue
• Muscles
• Facet joints, sacroiliaca joints
• Post/ant.longitudinal lig.• Periosteum vertebra (fascia,tendon,aponeurosis)
• Nerve roots• Blood vessels (spinal joint,sacroiliaca joint, verteb,
L-S muscles)
Estimated Prevalence of NeP
HAS/Neuro/RSHS-FKUP
Indonesia : 40% population, men>women hospital based : 3-17%
Low Back Pain
Triage diagnostik LPBTriage diagnostik LPB
LBP nonspesifikLBP nonspesifik SindromaSindroma radikulerradikuler KelainanKelainan patologik seriuspatologik serius
“ “ Red FlagsRed Flags “ “
(Agency for Health Care Policy and Research, Bigos 1994)(Agency for Health Care Policy and Research, Bigos 1994)HAS/Neuro/2005
Low Back pain
• Seriuos pathology: neoplasm
infection
fracture
cauda equina syndrome
• Ischialgia, radicular syndrome
• Nonspecific LBP
Low Back Pain
• Diagnostic triage• History taking and physical examination to
exclude red flags• Neurological examination (including
Lassegue test)• Consider psychosocial factors if there is no
improvement• X-rays, MRI ??
Red Flags of LBP
• Cancer
• Infection
• Vertebral fractur
• Cauda equina syndrome or
Severe neurological deficit
Yellow Flags
• Recognition of psychosocial factors
as predictors of chronicity and
obstacles to recovery
Acute subacute chronic
Risk Factors of LBP
• Physical : 35 – 55 y past history of LBP
• Occupational : vibration bending, twisting heavy lifting low job satisfaction
• Psychosocial : attitudes cognition fear-avoidance beliefs depression anxiety distress and related emotion
Management of acute LBP
• Diagnostic classification, D/ triage
• Reassurance
• Early and progressive activation
• Analgetics ?: acetaminophen
NSAID
consider muscle relaxants
• Recognition yellow flags
Management of Chronic LBP
• Behavioral therapy
• Education
• Intensive exercise therapy
Multidisciplinary
The International Classification of Headache Disorders ICHD 2 ( IHS 2004 )
The Primary Headaches Migraine Tension-type headache (TTH) Cluster headache Other primary headaches
The Secondary Headaches Headache attributed to head and/or neck trauma Headache attributed to cranial or cervical vascular disorders Headache attributed to non-vascular intracranial disorders Headache attributed to a substance or its withdrawal Headache attributed to infection Headache attributed to disorder of homoeostasis Headache or facial pain attributed disorder of cranial, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures Headache attributed to psychiatric disorders
Cranial Neuralgias, central & primary facial pain & other headaches Cranial neuralgias & central causes of facial pain Others headache, cranial neuralgias & central or primary facial pain
The International Classification of Headache Disorders ICHD 2 ( IHS 2004 )
The Primary Headaches Migraine Tension-type headache (TTH) Cluster headache Other primary headaches
The Secondary Headaches Headache attributed to head and/or neck trauma Headache attributed to cranial or cervical vascular disorders Headache attributed to non-vascular intracranial disorders Headache attributed to a substance or its withdrawal Headache attributed to infection Headache attributed to disorder of homoeostasis Headache or facial pain attributed disorder of cranial, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures Headache attributed to psychiatric disorders
Cranial Neuralgias, central & primary facial pain & other headaches Cranial neuralgias & central causes of facial pain Others headache, cranial neuralgias & central or primary facial pain
PAIN SENSITIVE CRANIAL STRUCTURES
• Skin,subcutan., muscle• Extracranial arteries• Skull periosteum• Eye,ear, nasal cavities,
sinuses• Intracran.venous sinuses,
large vein, pericavernous structures
• Basis dura, meningeal arteries, prox.ant/middle cerebral A, IC int.carotis A
• Superf.temporal A• Cranial nerves:II.III,V,IX,X,C1-
3
THE ROLE OF NEUROTRANSMITTER :THE ROLE OF NEUROTRANSMITTER : SEROTONIN (5 HT) SEROTONIN (5 HT) THE ENDOGENOUS PAIN CONTROL MECHANISM -> OPIOIDTHE ENDOGENOUS PAIN CONTROL MECHANISM -> OPIOID GABAGABA
MECHANISMS OF CRANIAL PAIN :
TRACTION ON OR DILATATION OF THE INTRACRANIAL
ARTERIES
DISTENTION OF EXTRACRANIAL ARTERIES
TRACTION ON OR DISPLACEMENT OF THE LARGE
INTRACRANIAL VEINS OR DURAL ENVELOPE
COMPRESSION, TRACTION OR INFLAMATION OF THE
CRANIAL AND SPINAL NERVES
SPASM, INFLAMATION & TRAUMA TO CRANIAL & CERVICAL
MUSCLE
MECHANISM OF CRANIAL PAIN (con’d)
DISEASE OF THE TISSUES OF THE SCALP, FACE, EYE,
NOSE, EAR AND NECK
MENINGEAL IRRITATION
INTRACRANIAL MASS LESION
RAISED INTRACRANIAL PRESSURE
LOWERED INTRACRANIAL PRESSURE : LP HEADACHE
ATTACK ONSET QUALITY SEVERITY LOCATION MODE OF ONSET TIME, INTENSITY, CURVE, DURATION CONDITION WHICH EXACERBATE / RELIEVE THE PAIN ASSOCIATED FEATURES SOCIAL HISTORY, FAMILY HISTORY PAST HEADACHE HISTORY HEADACHE IMPACT
HISTORY taking:
Faktor pencetus Nyeri Kepala
StresKurang/kebanyakan tidurTidak/telat makanBau menyengat : parfum,rokokLingkungan: cahaya silau/berkedip,gaduh ketinggian,panas,lembab ruang berasapMakanan/minuman
HAS/Neuro/Bdg/04
Secondary Headache Red Flags “SSNOOP”
• Systemic symtoms (fever, weight loss) or• Secondary risk factors : underlying diseases
(HIV,systemic cancer)• Neurologic symtoms or abnormal signs (confusion,
impaired alertness,or consciousness)• Onset: sudden,abrupt, or split-second (first,worst)• Older: new onset and progressive headache, especially
in middle age>50 (giant cell arteritis)• Previous headache history or headache progression:
pattern change, first headache or different
(change in attack frequency, severity, or clinical pictures)
Tension Type Headache
• Psychologic factors• Muscle contraction and myofacial tenderness• Vascular factorsn : NO• Humoral factors : 5HT• Central factors : central pain control system
HEADACHE TREATMENT
• PRIMARY HEADACHE TREATMENT
Abortive
Preventive
• SECONDARY HEADACHE
TREATMENT
Causal Symtomatic : Analgesic
PRIMARY HEADACHE TREATMENT
TTHAbortive :Simple analg : acetaminophen/
ASA/NSAID
Preventive : Amitriptylin
Nonpharmacologic therapy
MIGRAINEAbortive :Simple analg : acetaminophen/
ASA/ NSAIDSpecific analg : ergot alkaloids ( ergotamine/ DHE )/ triptanAntiemetics : metoclopramide/
domperidone
Preventive : Anticonvulsants / Adrenoceptor blockers (propranolol)/ Antidepressants/ Ca-channel blockers
Nonpharmacologic therapy
CLUSTER HA
abortive : – o2 inhalation– ergot alkaloids, – triptans
preventive : – verapamil– ergot alkaloid
Cranial Neuralgias,Central Pain
(Neuropathic Pain) Treatment • Antidepressants• Anticonvulsants• Antiarrhitmic• Local anesthetic
Penanganan tanpa obat
EdukasiMengenal & menghindari faktor pencetus
Modifikasi perilakuLatihanRelaksasiBiofeedbackTerapi perilaku kognisiTerapi fisik
TENS (transcutaneus electric nerves stimulation)
HAS/Neuro/Bdg/04