NAIOMT May 2010 Symposium
The term ‘Facilitated Segment’ was first introduced by Irvin Korr in 1947 (Korr IM 1947) and supported by his co-worker Denslow J (Denslow JS et al 1947).
The original model proposed was extremely simple. Repetitive, abnormal input of afferents from spinal structures and/or visceral structures would converge on the same segment of the spine. This repeated bombardment would decrease ‘synaptic resistance’ thus making transmission of impulses to the efferent system (skeletal muscle and viscera) easier, i.e, ‘facilitated’.
This would allow lesser degree of afferent input to have a greater efferent output.
This simplistic model was to explain skeletal muscle hypertonicity but also how spinal dysfunction can alter the sympathetic outflow. Apart from trophic changes in segmental skin it was also proposed that altered sympathetic outflow could directly and deleteriously affect systemic organ function.
Since the sympathetic system controls arterial function, for many Osteopaths this theory was validation of Andrew Still’s original concept of ‘The Law of the Artery’ in 1892.
In the early 1980’s Physical Therapy education was being significantly influenced by the Osteopathic profession’s view of neurophysiology. However, from the mid-1980’s many Physical Therapy publications had begun to put forward significant challenges to the concept of ‘The Facilitated Segment’ (Kukulka C 1986; Leone J and Kukulka C 1988; Belanger A 1989; Sullivan S 1991 and 1993).
Criticism also came from within Osteopathy itself (Newham D and Lederman E 1993; Lederman E 1997; Lederman E 2000).
In 2000 Lederman D.O. published a paper within the British Osteopathic Journal and contained the following summary: “In my view the principle of the ‘Facilitated Segment’ has stifled the development of osteopathic neurophysiology for the last 50 years”.
Despite such opposition eminent Osteopaths such as John Upledger remain undaunted. As recently as 2003 Upledger (Upledger J 2003) reinforces the concept of organic dysfunctions secondary to spinal facilitated segments: the heart (T4); stomach (?); gall bladder (T9/10); kidneys (T12/L1); urino-genital (L5).
In this same paper Upledger states that chronic facilitated segments ‘…can continue for years, even contributing to death’.
More modern concepts:
Historically the medical profession has always rejected the Osteopathic claim to be able to treat disease through spinal manipulation. The theoretical model of the facilitated segment would be no exception.
However, medical researchers have always been interested in the phenomena of referred pain and explain it within the neurophysiological model of ‘central sensitization through convergence’ (Bogduk N 1994).
The principles behind central sensitization may initially sound similar to those of the facilitated segment, but with some important differences.
In reviewing the neuroanatomy involved it is recognized that afferent sensory pathways can be divided into 2 main categories: visceral and somatic.
The vast majority of visceral afferents are physiologic. These include baro-receptors, chemo-receptors, cough receptors and receptors from the abdominal and pelvic viscera. Their functions are obviously autonomic control of the body to maintain healthy stasis. They synapse in the lateral horn with pre-ganglionic motor fibres of the sympathetic system.
A very small number of sympathetic afferents are known as ‘silent’ afferents. They arise from visceral nociceptors whose main function is to relay abnormal activity within organs e.g, inflammation, ischaemia. The important thing is that they, unlike their physiologic counterparts primarily synapse in the substantia gelatinosa.
This is the ‘sorting house’ of ALL somatic sensory/nociceptive and visceral nociceptive information from the entire body. Above C2/3 this region expands and becomes known as the cervical nucleus of the trigeminal system.
The substantia gelatinosa (so-called because it houses predominantly cell bodies giving it a gelatinous consistency) is designed as a cellular interactive region with 1st order neurones. It has 8 laminae transversely, but its vertical orientation has not yet been accurately mapped.
Afferent neurones tend to target specific laminae, e.g, A delta fibres target lamina I and V. C fibres target lamina II. A beta fibres target lamina IV etc.
However, there is a tremendous amount of lamina interaction, especially targeting lamina V.
Recent research shows that abnormal segmental afferent input encourages axonal ‘sprouting’ towards lamina V (horizontally, as well as vertically).
This model sets up the explanation for segmental and extra-segmental reference of pain. If the predominate abnormal input is from visceral nociceptors then the resulting pain will appear to be extra(muti)-segmental reference e.g, cardiac pain.
As much as the medical research concept of central excitation has elucidated the causes of musculo-skeletal or visceral pain why doesn’t it validate Korr’s concept of the facilitated segment?
Whilst sensory interactions between abnormal afferent visceral input and referred pain is scientifically acceptable through the theory of convergence and central sensitization, no similar visceral ‘convergent theory’ has been demonstrated regarding organic dysfunction.
Far from it, since abnormal spinal, segmental sensory input has its effect via the substantia gelatinosa, such a connection has yet to be shown from non-nociceptive (visceral sensory) input. Furthermore, sympathetic motor outflow is so multi-segmental i.e, DIVERGENT not convergent, that its neurophysiological impact would be minimal and unlikely to have a significant impact in visceral function.
The model of convergence and central sensitization adequately explains the genesis of segmentally and viscerally referred pain.
So how does this model of central sensitization relate to muscular function?
The ‘electrical depolarization’ model and the concept of ‘synaptic facilitation’ seems to be shared by both theories. Recent research shows that ACH density remains higher within the synapse if the rate of conduction is increased. This tends to endorse at least that part of Korr’s concept ie., decreased synaptic resistance. It would seem logical that both alpha and gamma motor neurons would be centrally sensitized.
Unlike referred pain this aspect of sensitization has received scant research attention (Korr I 1962; Patterson MM 1976; Johansson H 1988).
However, consistent clinical findings (at least from the writer’s perspective) are that segmental spinal dysfunctions are accompanied by both segmental spinal muscle hypertonicity and changes within peripheral muscles. Such changes include ‘tightness’ or resistance to stretch, and tenderness upon palpation.
I propose the following model to explain these clinical findings.
If this model were correct then it may be used to help more clearly define some difficult terms.
During a literature search it was obvious that the term ‘hypertonicity (hypertonus)’ is constantly being used in the same sense as ‘spasm’ and ‘spasticity’.
The term ‘exaggerated reflexes’ is often confused with ‘hyper-reflexia’.
Using the proposed model, increased ALPHA MOTOR NEURON sensitization would produce:
HYPERTONUS defined as ‘recruitment of an excessive number of motor units at rest’. This would lead to:
- increased palpatory ‘firmness’ of muscle
- increased resistance to stretch (lengthening)
- exaggerated response to a deep tendon reflex test
INCREASED GAMMA MOTOR NEURON TONE. This would lead to:
- increased sensitivity to deep tendon reflex tests (exaggerated response)
- increased resistance to rapid stretch. ? predisposing to muscle tears.
Central sensitization of the C6 segment has commonly given PT’s the challenge of the ‘pseudo’ tennis elbow which adequately demonstrates all the above mentioned phenomena. In addition, however is the presence of tenderness to palpation of the ecrb muscle belly and its origin at the epicondyle.
Also, frequently there is increased pain with isometric resistance of wrist extension (? sensitivity to stretch of the periosteum) that decreases with successively repeated tests. This decrease in sensitivity probably represents increased activation of ‘A fibre’ input affecting the ‘gating mechanism’.
AXONAL and NEURONAL TRANSPORT
In 1980 a paper written by James Schwartz (Schwartz JH 1980) was about to change our understanding of nerve function forever, though few would appreciate its importance at that time.
Prior to 1980 most viewed the axon of a nerve as a clear, fluid-filled tube that supported the myelin sheaths and accommodated the sodium/potassium pump i.e, it’s predominant function was to assist in the transmission of an electrical impulse.
What Schwart’s paper illustrated was that a nerve axon had (at least) two functions. One, to facilitate electrical nerve conduction and a second, the transport of chemical substances.
His electron microscopic studies showed that the axon contained a multitude of longitudinal molecular rods and microtubules supported by mitochondria, lysosomal and other bodies.
What Swchartz had discovered was to be the foundation of 30 fascinating years of research in what is now known as axonal transport.
Around the 5th week of embryological development immature neuroblasts from the neural crest are attracted to their ‘target cells’ by chemotaxis. They achieve this by sending out ‘microspikes’ from the growth cone. When the neuroblasts reach their target cells chemistry from their target cells enable their ‘target cells’ to reach histological and functional maturity. It appears that this chemical interaction and interdependence will then be maintained for a lifetime.
The axoplasm of the axon is being continuously replaced by the cell body. Its rate of flow is approximately 1mm per day. When an axon is cut or injured it repairs at this same rate, arising from axoplasmic projections (cf. Wallerian regeneration).
Axonal transport of chemistry occurs in both directions (Tsukita 1980) i.e, away from the cell body (anterograde transport) and towards the cell body (retrograde transport).
The most obvious function of this two-way transport system is to replenish the chemistry of synaptic vesicles i.e, the neurotransmitters (e.g, acetylecholene) and then ‘recycle’ the bi-products of synaptic interaction. This replenishment, of necessity, is extremely fast and measured in m/sec. Other molecules are transported much more slowly (mm/day), but these apparently have an extra-cellular destination.
Health of a neuronal cell is directly dependent upon axonal transport i.e, retrograde chemical input from its target cells is essential for its existence (Saper CB 1987; Jablonka S 2004; McMartin DN 1979).
On the other hand chemistry produced by the neuronal cell body (anterograde transport) is essential for normal function of the neuron’s target cells (e.g, muscles cells) (Boegman RJ 1980; Munoz-Martinez EJ 1981).
Therefore, axonal chemical transport takes on a very important role.
We already know that axonal transport, or rather dysfunctions in axonal transport, are responsible for, or a contributory factor in many of our recognized neurological dysfunctions ranging through Herpes, HIV, Parkinsons Disease ,etc (Ashmed F 2009; McGraw HM 2009; Mitchell CS 2009; Ohka S 2003; Rothstein JD 2009).
For us as manual therapists, how is axonal transport relevant?
Chemicals transported via the axon are not exclusive to synaptic function or neuronal cell health. They include substances that are utilized by the neuromuscular junction and the muscle cells themselves (actin and myosin).
If axonal transport is slowed or stopped there are serious consequences for the normal function of the neuron’s target cells including deterioration of the motor endplate (Ashmed F 2009; McGraw HM 2009; Mitchell CS 2009; Ohka S 2003; Rothstein JD 2009). Muscle tissue itself will rapidly waste and weaken (Holzbaur EL; McMartin DN 1979).
What can cause a decrease in axonal transport?
Pressure or distraction forces will obviously disrupt axonal transport, regardless of whether it disrupts electrical nerve conduction (Feany M 2003; Flak M 2006; Martin JE 1990; Maxwell WL 1997) i.e, a muscle can initially still maintain its strength of contraction whilst eventually becoming structurally weaker.
This is especially important to understand when considering psoas.
Instability of L5/S1 will create an abnormal tension within the ilio-lumbar ligaments. Since these structures are derived from the myotomes of L2, the L1/2 and L2/3 segments will become centrally sensitized.
Between resultant hypertonus of psoas, and an inevitable decrease in axonal transport to its motor endplate and its muscle tissue, the psoas will ultimately become hypertonic (resisting stretch) and WEAK.
The last thing such a muscle requires is the brutality of passive stretching. What it does require is neurological balancing, strengthening and co-ordination.
Decreased blood supply will also adversely affect both axopasmic flow and axonal transport (Hides JA 2007; McLeod D 1975). Such segmental ischaemia has long been recognized as a consequence of severe spinal spondylosis.
We can now better understand the presence of segmental or multisegmental weakness occurring in the absence of any sign of direct nerve root pressure.
How does ‘central sensitization’ affect axonal transport?
With regard to central sensitization one would assume that increased electrical activity would necessitate a corresponding increase in axonal transport. However, it has been shown that non-volitional increased electrical activity (reflex hypertonicity) actually decreases axonal transport (Lardong K 2009). This doesn’t seem to make sense since increased synaptic activity demands an increase in chemical support.
We see what might be viewed as a clinical oxymoron.
Central sensitization creates hypertonus within spinal segmental and peripheral key muscles. This means that initially a muscle is strong and resists stretch. Chronically, the affected muscles will become both electrically and structurally weak.
Clinical observation suggests that although hypertonic muscles do not necessarily get stronger they do tend to neurologically inhibit their functional antagonists. This certainly fits with the work of Vladamir Janda.
So let’s look at a chronically hypermobile (unstable) lumbo-sacral junction (L5/S1).
It has been demonstrated that the most immediate affect is weakness and wasting of the deep segmental stabilizers (cervical spine also) (Barker KI 2004; Fernandez-de-las-Penas C 2008; Hides T 2008; Hodges P 2006; Hyun JK 2007).
There also exists a pattern of (?central and unexplained) inhibition that at least, includes the pelvic floor and abdominals (Hodges P; Jull G).
If our model of central sensitization is correct then the functional antagonists to psoas will be inhibited and ‘electrically’ weak (i.e, they can be strengthened by neurological ‘facilitation’ of increased motor unit recruitment).
During gait the functional antagonist to psoas is the opposite ‘lateral pelvic wall’ muscles, predominantly ‘femoral’ glut max and piriformis, but generally the short lateral rotators of the hip.
On a stable femur the femoral part of glut max and piriformis produce sacral counter-nutation, thus maintaining the L/S and SIJ neutral zone. Their weakness now perpetuates the existing lumbo-sacral instability.
So the chronic picture is as follows:
- Weak and wasted segmental multifidus
- Inhibited and weak pelvic floor and abdominals
- Hypertonic and weak psoas
- Inhibited weakness of the short lateral rotators of the hip.
Before we rush into strengthening anything let us remember that central sensitization and resultant decreased axonal transport began with a lumbo-sacral instability chronically irritating ligaments.
The priority is clear. Keep the lumbo-sacral junction in neutral. The method? Well, that just begins another debate, but what is clear is that we have to prioritize the order in which muscle groups are facilitated/strengthened and this will be dependent upon the clinical findings and functional demands of the individual patient.
References for the ‘Facilitated Segment’:
Denslow JS et al 1947 Ouantitive studies of chronic facilitation in the human motoneuron pool. In: The collected papers of Irvin M. Korr. B. Peterson (ed). American Academy of Osteopathy, Colorado, 18-21
Korr IM 1947 The neural basis of the osteopathic lesion. In: The collected papers of Irvin M. Korr. B. Peterson (ed). American Academy of Osteopathy, Colorado, 120-127
Upledger J D.O. (Massage Today. Jan 2003; Vol.03 Issue 01).
*Lederman E 2000 Facilitated segments: a critical review. British Osteopathic Journal 22:7-10.
Lederman E 1997 Fundamentals of manual therapy: physiology, neurology and psychology. Churchill Livingstone, London
Belanger AY, Morin S, Pepin P, Tremblay M-H, Vacho J 1989 Manual muscle tapping decreases soleus H-reflex amplitude in control subjects. Physiotherapy Canada, 41:4:192-196
Goldberg J 1992 The effect of two intensities of massage on H-reflex amplitude. Physical Therapy 72:6:449-457.
Kukulka CG, Beckman SM, Holte JB, Hoppenworth PK 1986 Effects of intermittent tendon pressure on alpha motoneuron excitability. Physical Therapy 66:7:1091-1094
Leone JA, Kukulka CG 1988 Effects of tendon pressure on alpha motoneuron excitability in patients with strokes. Physical Therapy 68:4:475-480
Newham DJ, Lederman E 1997 Effect of manual therapy techniques on the stretch reflex in normal human quadriceps. Disability and Rehabilitation 19:8:326-331.
Sullivan SJ, Williams LRT, Seaborne DE, Morelli M 1991 Effects of massage on alpha neuron excitability. Physical Therapy 71:8:555-560
Sullivan SJ Seguin S, Seaborne D, Goldberg J 1993 Reduction of H-reflex amplitude during the application of effleurage to the triceps surae in neurologically healthy subjects. Physiotherapy Theory and Practice 9:25-31
Korr et al. 1962. J Neural Transmission 23(23):330-335.
Patterson MM 1976. A model mechanism for segmental facilitation. J Am Osteopath Assoc 76:62.
Johansson H. 1988 Different fusimotor reflexes from the ipsi and contralateral hind limbs of the cat……. J Physiol (Paris) 83(4):28192
Bogduk, N 1994. ‘Cervical causes of headache and dizziness’.
Grieve’s Modern Manual Therapy. The Vertebral Column. 2nd Ed. Churchill Livingstone, Edinburgh. Chapter 22, p317-331.
References for ‘Axonal Transport’
Schwartz JH. 1980. The transport of substances in nerve cells. Sci Am.1980 Apr, 242(4):152-171.
Ann Neurol.2009 Jan; 65 Suppl 1:53-9
Defective axonal trans implicated in ALS
Mitchell CS, Lee RH
J Theor Biol. 2009 Apr 7; 257(3): 430-7
Ahmed F, MacArthur L, De Bernard MA, Mochetti I.
Brain Behav Immun. 2009 Mar; 23(3): 355-64
Axonal transport exacerbates pathogenisis of HIV
Maxwell WL, Graham DI.
J Neurotrauma. 1997 Sept; 14(9): 603-14
Loss of axonal microtubules and neurofilaments following stretch injury to n fibres.
Martin Je, Mather KS, Swash M, et al.
Brain. 1990 Oct; 113 (P+5): 1553-62.
Following spinal cord trauma, loss of axonal transport leads to changes in neural proteins not seen in neural disease
FeanyMb, La Spada AR.
Neuron. 2003 Sept 25; 40(1): 1-2.
Polyglutamines proteins (polyQ) lead to neurodegenerative diseases thro’ blocking rapid axonal transport
Ohka S, Sakai M, Bohnert S, et al
J Virol. 2009 Feb 25. (Epub)
Polio virus transmitted through rapid retrograde axonal trans.
Saper CB, Wainer BH, German DC.
Neuroscience. 1987 Nov; 23(2): 389-98.
Axonal transportneeded for neural cell health. Disruption facilitates neurodegen diseases like Alzheimer’s.
McGrawHM, Friedman HM.
J Virol. 2009 Mar 11. (Epub)
Herpes simplex spread by retrograde axonal transport.
Lardong K, Maas C, Kneussel M.
Neuroscience. 2009 Feb 27 (Epub)
Induced increased neural activity inhibits axonal transport. Inhibition doesn’t.
Munoz-Martinez EJ, Nunez R, Sanderson A.
J Neurobiol.1981 Jan; 12(1): 15-26
Decr axonal transport affects chemistry of neuromuscular synapses.
Tsukita S, Ishikawa H.
J Cell Biol. 1980 mar; 84(3): 513-30.
Anterograde and retrograde transport structured differently for different functions.
Lancet. 1975 Nov 15; 2(7942): 954-6.
Decr vascularisation leads to decr axonal transport.
Boegman RJ, Deshpande SS, Albuquerque EX.
Brain. 1980 April 7; 187(1): 183-96.
Changes in transmitter subs at neuromusc junction affected by decr axonal trans NOT by decr electrical depolarisation.
Trends Cell Biol. 2004 May; 14(5): 233-40
Defective axonal trans leads to ms atrophy
Jablonka S, Wiese S, Sendtner M.
J Neurobiol. 2004 Feb 5; 58(2): 272-86.
Decr axonal transport leading role in human motor neuron disease.
McMartin DN, O’Connor JA Jr.
Mech Ageing Dev. 1979 May; 10(3-4); 241-8.
Atrophy of ms in ageing linked to decr in axonal transp.
Wallwork TL, Stanton WR, Freke M, Hides JA.
Man Ther. 2008 Nov 20.
Segmental atrophy of multif in chronic LBP
Fernandez-de-las Penas C, Albert-Sanchis JC, Buil M, et al.
J Orthop Sports Phys Ther. 2008 Apr; 38(4): 175-80.
Atrophy of cerv ms in females with chronic neck pain.
Hyun JK, Lee JY, Lee SJ, Jeon JY.
Spine. 2007 Oct 1; 32(21): E598-602.
Unilateral seg wasting in multif in PLP.
Hides JA, Belavy DL, Stanton W, et al.
Spine. 2007 Jul 1; 32(15): 1687-92.
8wks bed rest (10 healthy males) – atrophy of multif with incr strength in flexors – ? decr blood flow due to decr activity.
Hodges P, Holm AK, Hansson T, Holm S.
Spine. 2006 Dec 1; 31(25): 2926-33
Induced disc lesion (pigs) led to localised segm atrophy of multif. Nerve lesion of L3 dorsal ramus led to generalised atrophy.
Hides T, Gilmore C, Stanton W, Bohlscheid E.
Man Ther. 2008; 13(1):43-9
Greatest multifidus wasting at segmental level of injury.
Barker Kl, ShamleyDR, Jackson D.
Spine. 2004 Nov15; 29(22): E515-9
Atrophy of multifidus is segmental and ipsilateral.
Flak M, Durmala J, Czernicki K et al.
Stud Health Technol Inform. 2006; 123:435-41.
‘Double crush study’. Pts with chronic neck pain ms atrophy – 43% of ms proximal to susp site and 70% distal to site. No overt palsies detected.
Textbooks of Neuroanatomy and Neurophysiology
Haines D. Fundamental Neuroscience for Basic and Clinical Applications. 3rd Edn. Churchill Livingstone.
Kandel E, Schwartz J, Jessell T. Principles of Neural Science. 4th Edn. McGraw Hill.
Gray’s Anatomy. (British edition) 39th Edn. Editor-in-chief Standring S. Elsevier Churchill Livingstone.