Central Nervous System Pain Control PDF

Central nervous system By Dr : Basma Helal Lecturer of physiology  Pain control (analgesia) system The degree to which a person reacts to pain varies. This result partly from the capability of the brain to suppress pain impulses carried by pain pathway via act...

Central nervous system By Dr : Basma Helal Lecturer of physiology  Pain control (analgesia) system The degree to which a person reacts to pain varies. This result partly from the capability of the brain to suppress pain impulses carried by pain pathway via activating a pain control system or analgesia system. Pain control (analgesia) system includes: I. Pain control at higher central level. II.Pain control at spinal cord level. (I) Pain control at a higher central level: In CNS, pain suppression is present at different levels. Each level contains opiate receptors and secretes opioid peptide (have morphine like action). This is the mechanism by which a soldiers wounded in a battle may feel no pain until the end of battle  this is called stress analgesia.  The analgesia system at higher central level includes: (1) Hypothalamus & limbic system: As a result of severe stress and emotional stimuli the hypothalamus secretes opioid peptide endorphin. (2) Preaqueductal gray matter:  It is present in the mid brain and upper pons.  It contains opioid receptors stimulated by endorphin coming from the hypothalamus.  It secretes opioid peptide enkephalin. (3) Raphe magnus nucleus:  It is present in the lower pons and upper medulla.  It contains opioid receptors stimulated by enkephalin coming from the preaqueductal gray matter.  It secretes opioid peptide serotonin. (4) Pain inhibitory complex (PIC):  It is present in the dorsal horn of the spinal cord.  It is composed of small inhibitory interneurons which synapse with terminal afferent A fibers (carry fast pain) or with terminal afferent C fibers (carry slow pain).  PIC contains opioid receptors stimulated by serotonin coming from the Raphe Magnus nucleus.  PIC secretes opioid peptide enkephalin.  Enkephalin blocks the calcium channels in the terminal part of the afferent sensory fibers producing presynaptic inhibition  so, preventing release of pain producing substances from terminal part of sensory afferent carrying pain sensation.  So, PIC blocks transmission of pain impulses at initial entry point in dorsal horn of the spinal cord (SGR). This is called spinal gate (II) Pain control at the spinal cord level: 1.A beta fibers which are afferent fibers of gracile & cuneate tracts:  They send collateral to end at small inhibitory neurons of PIC lead to its stimulation  causing presynaptic inhibition & closing the spinal gate and block pain transmission.  This explained by rubbing skin around painful area relief pain from this area. 2.A delta fibers which are the afferent of pricking pain:  They send collateral to end at small inhibitory interneurons of PIC causing presynaptic inhibition block pain transmission.  This is explained by the relief of pain in cases of acupuncture and counterirritant drugs.  Some clinical abnormalities of somatic sensations I. Cutaneous hyperalgesia: Definition: It is a pathological condition where pain sensation from skin is abnormally exaggerated.  Types: 1- Primary hyperalgesia: 2- Secondary hyperalgesia: 1- Primary hyperalgesia:  It is a pathological condition of skin in which pain is produced by non noxious stimulus.  It occurs in affected skin area & the surrounding area of redness around the site of injury.  Pain threshold is lowered (non painful stimuli become painful) and painful stimuli become exaggerated.  Its mechanism: It is due to sensitization of pain receptors by accumulation of pain producing substances (histamine, substance P & prostaglandins) that released from damaged tissues. 2- Secondary hyperalgesia: It a pathological condition of the skin in which noxious stimuli produce prolonged and exaggerated pain than normal. It occurs in normal healthy skin area around area of primary hyperalgesia. Pain threshold is normal or elevated. But, pain sensation is prolonged and severe.  Mechanism of secondary hyperalgesia: Convergence facilitation mechanism: Impulses from area of primary hyperalgesia and impulses from area of secondary hyperalgesia converge on the same SGR. Impulses coming from area of secondary hyperalgesia are facilitated by impulses coming from the primary injured area. N.B.: Secondary hyperalgesia in the skin can occur in absence of primary hyperalgesia as in some cases of visceral and deep pain (in which the facilitatory impulses are discharged from the diseased viscus or deep tissue). II. Syringomyelia: It is slowly progressive disease that is congenital in origin. It affect mainly middle aged females. It is characterized by cavity formation of gray matter around central canal of spinal cord , lead to compression and damage of crossing fibers of spinothalamic sensation ( pain, temperature, crube touch ) in both sides. The lesion usually occurs in lower cervical and upper thoracic segments. ◼ Manifestations: 1. Loss of pain and temperature on both sides of body at the level of affected segments:  It is due to damage of lateral spinothalamic tracts where they cross around the central canal.  This loss has a Jacket distribution (because lesion usually in cervical and upper thoracic segments). 2. Sensations transmitted by dorsal column are not affected (e.g. fine touch, vibration, proprioceptive sensation) because dorsal columns do not cross in spinal cord. 3. Crude touch is diminished (but not lost), although the ventral spinothalmic tracts are damaged, because this sensation is transported to some extent by dorsal column tracts. III. Tabes Dorsalis: It is a nervous disease caused by syphilis. Which result in gradual compression of the dorsal roots central to dorsal root ganglia. Gracile and Cuneate tracts degenerate. The dorsal roots are mostly affected in thoracic and lumbosacral regions. Manifestation of the disease: (I)Early manifestations: 1. Attacks of severe pain due to irritation of pain afferent fibers. 2. Loss of fine touch, proprioceptive sensations and vibration sense, due to damage of Gracile and Cuneate tracts (because thick A β fibers are affected easily by compression). 3.Loss of proprioceptive sensations leads to  sensory ataxia.  Sensory ataxia means incoordinated voluntary movement as a result of loss of sense of position and movement.  Sensory ataxia is characterized by: (a)Positive Romberg’s sign: (it means that patient tends to fall if he closes his eyes). (b)Stamping gait: During walking, patient raises his legs too high and drops them strongly on the ground. (c)The patient walks at a broad base and often looks at his feet. (II) Late manifestations: 1) Loss of pain and temperature in region supplied by the affected dorsal roots. 2) Slow pain remains intact for long periods (because it carried by the thin C fibers that resist compression). 3) Loss of all reflexes: as following i) Superficial somatic reflexes. ii) Deep somatic reflexes: as stretch reflex resulting in loss of muscle tone & tendon jerks. iii)Visceral reflexes: (e.g. micturition, defecation & erection reflexes). This occurs if sacral roots are damaged bilaterally  leads to retention with overflow.