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The case of a non-traumatic sprained ankle
Manual Therapy (1999) 4(3), 163±168 # 1999 Harcourt Publishers Ltd
Case report
The case of a non-traumatic sprained ankle C. Uth School of Healthcare Professions, University of Brighton, Sussex, UK
alteration of the sensory and motor functioning of the target tissues. An alteration of the axoplasmic ¯ow has further importance in terms of the nutrition of the nerve and if the ¯ow is diminished, it will leave the peripheral part of the nerve vulnerable and prone to injury (Butler 1991). Furthermore, Butler (1991) suggested that a restriction of the axoplasmic ¯ow might cause trophic changes in the target tissues such as muscle and skin, causing damage to cell bodies and the axon. He suggested that this damage could be a possible explanation for injuries such as an Achilles tendon tear or lateral epicondylitis. In¯ammation of a nerve may lead to an irritation of the free nerve endings of the nervi nervorum (Greening & Lynn 1998a). The pain sensation from an in¯amed nerve is often described as causing bizarre or unfamiliar symptoms, examples are a burning or a crawling sensation (Butler 1991). Laminar nerve root compression is a common consequence to spondylolisthesis (Grieve 1988). Nerve root compression may also be due to an in¯ammation of extra neural soft tissue such as intervertebral disc, fat tissue, ligaments and joint capsules causing pressure on the nerve (Butler 1991).
INTRODUCTION Signs and symptoms originating from the nervous system may be far more common than we are aware of in our daily clinical work. Compression of a peripheral nerve can lead to neuropathy causing alterations in sensation and/or strength in areas distant to the location of the injury or to a neuropathy, with pain as the response from the peripheral nerve system (Butler 1991). Compression is most likely to happen in areas where there is limited room for oedema to escape or where mechanical pressure directly compresses the nerve at the soft tissue and/or bony interfaces (Butler 1991). A local distal neuropathy may be particularly aggravated when a provocation is directly applied to the area, yet the cause of the symptoms might be a compression located more centrally, e.g. at the root of a peripheral nerve. This can easily lead to a confusion as to which structure is causing the symptoms. The successful rehabilitation will, in cases like these, depend on the treatment of the underlying pathology, for example at the nerve root. Long-standing compression of a peripheral nerve does not necessarily cause clinical changes, such as an alteration in sensation and/or a decrease in muscle power (Grieve 1988), and a nerve root compression alone is not painful (Grieve 1988). A nerve can withstand severe compression without changes in conduction or pain response. Greening and Lynn (1998a) argued that both in¯ammation and compression of a nerve root could cause decreased nerve conduction. Chronic compression is thought to be a source of nerve root in¯ammation and an in¯ammatory process causes changes such as local ischaemia, oedema, ®bre deformation, entrapment and ®brosis (Grieve 1988). The ®brosis, as well as the oedema, restricts the axoplasmic ¯ow, which is important for the conduction of the nerve. This may lead to an
SUBJECTIVE EXAMINATION The patient concerned in this case report was a 38year-old woman, diagnosed by her General Practitione (GP) with a ``sprained ankle''. She presented herself for treatment with symptoms, which had started 4 weeks prior to the physiotherapy consultation. The onset of the symptoms began whilst walking; she experienced a sudden sharp, unprovoked pain at the lateral side of her left ankle, which she rated as being 6 out of 10 on a visual analogue scale (VAS) (Scott & Huskisson 1979). She consulted her GP on two occasions over the following 4 weeks, complaining of lateral ankle pain. This swelling was diagnosed as a sprained ankle and she was told that her symptoms would heal within a couple of weeks.
Carsten Uth, DipPhty (Den.), MCSP, 10 Walcot Court, 1B Ashburton Road, Croydon CR0 6AP, UK. 163
164 Manual Therapy
This diagnosis was given in spite of the fact that she had not experienced any twisting of her ankle. As the ankle had not improved satisfactorily after almost 4 weeks, she contacted our physiotherapy clinic. Over the previous 4 weeks, she had been able to play tennis with low intensity on two occasions, experiencing some left ankle pain. Wearing an ankle support eased this. The swelling had decreased by 90% over the previous couple of days and as her GP had told her that her ankle would recover by itself, she almost felt ashamed to seek help, despite stiness and some pain in the ankle. At her ®rst visit to the clinic, her main complaint was stiness of the left ankle, a dull ache, which she rated as 0.5 out of 10 on a VAS and that the foot did not `feel right' (Fig. 1.) Pain was aggravated when depressing the clutch of her car and this decreased as soon as the clutch was released. In sitting, circling her left foot in the air produced the stiness and pain she complained of in her left ankle. This function was chosen as a subjective marker. During walking, sitting and standing she was free of pain. Her previous medical history included an injury to the left lower leg and proved to be of relevance to the current problem. Approximately 10 years ago she had experienced an almost complete tear of her left Achilles tendon at the end of a recreational tennis game. This was treated with 5 weeks in plaster followed by physiotherapy rehabilitation over a 3 week period. She had since had three children and with each pregnancy, she had experienced clear atrophy of her left triceps surae muscles. She could not recall any severe lower back pain. She had received physiotherapy treatment for this muscle
wasting at another physiotherapy clinic and it had been explained to her that the hormones released during pregnancy, to enable the birth passage to increase, were responsible for the weakening of her ligaments. She was told that this hormone release was also responsible for the weakening of her left Achilles tendon, thereby causing muscle weakness of the left calf muscle. She was rehabilitated with strengthening exercises and recovered fully after each birth. Special questions (Maitland 1986) only revealed a tendency to epilepsy for which she took one mild epilepsy tablet on a daily basis. During the previous 10 years, she had only experienced four mild attacks.
INITIAL IMPRESSION AFTER THE SUBJECTIVE EXAMINATION The initial impression following the subjective questioning indicated that signs and symptoms of her presentation did not ®t together. She complained of lateral ankle pain, which her GP had diagnosed to be a twisted ankle. The structures of the ankle would have to be investigated, but lack of injury to the local area suggested that more central ± neural structures would have to be investigated too. Tearing of the Achilles tendon had happened 10 years ago, which meant that she would have been 28-years-old at the time. Mandelbaum et al. (1995) referred to reports showing that 75% of Achilles tendon injuries occur in athletes, predominantly men between 30 and 40 years of age. A rupture at the age of 28 in a female might therefore be an unusual phenomenon and could possibly be linked to Butler's suggestions (1991) that altered axoplasmic ¯ow creating trophic changes in muscles and tendons may cause tears like these. The patient's muscle atrophy of her left calf muscle during her three pregnancies could furthermore indicate altered nerve conduction. A thorough assessment of her lower back and neural structures was indicated. Her previous physiotherapists had suggested that her calf muscle atrophy could be linked to the release of hormones ± this explanation was found to lack support. If the wasting was related to hormones, such symptoms would have been more widespread in the body (Sandler 1996).
PHYSICAL EXAMINATION Observation
Fig. 1ÐBody chart with the distribution of pain. Manual Therapy (1999) 4(3), 163±168
It was noted that the patient had a ¯attish spine, a slight right convex scoliosis in the thorax area, decreased left calf muscle bulk and a thickened left Achilles tendon with postoperative scar tissue at the lateral part of the tendon. In general, she was tall and thin with a tiny physique; an ectomorph. # 1999 Harcourt Publishers Ltd
Case report 165
Lumbar spine movements Extension appeared restricted by approximately 50% due to stiness. Flexion was unremarkable, as were lateral ¯exion and rotation to each side. Gait Her pain was reproduced when walking on her toes. It was also noted that her scoliosis increased during stance-phase on her left leg during normal gait. Dynamic tests A lunge test indicated that she had approximately 15% increased range of movement in her left ankle dorsi¯exion, with the knee both straight and slightly ¯exed, indicating an increased length of both gastrocnemius and soleus. Neurological tests All sensation, muscle strength and re¯ex tests of the left leg were comparable to the non-involved side. Neurodynamic tests Straight Leg Raise (SLR) was, on both legs, restricted by resistance at approximately 60 degrees and produced no symptoms. When her left ankle was inverted to nearly end of range her pain was exactly reproduced. Furthermore, this pain was increased with cervical ¯exion. This was chosen as an additional marker. No pain was produced on inversion of her right foot in SLR. Passive movement tests Physiological dierentiation movements of the ankle and foot indicated that inversion was the aggravating factor. Various tests (Kaltenborn 1989; Maitland 1991) of the ankle and lower leg joints were performed and all individual joints were found normal. The hip and knee joints were all normal too.
Palpation and Passive Physiological intervertebral Movements (PPIVM) of the lumbar spine Passive accessory intervertebral movement examination of her lumbar spine showed that her lumbar spine was very sti on unilateral palpation bilaterally over the facet joints from the L3 to L5. Furthermore, pain was elicited on unilateral pressure applied to her left L5 transverse process. The movement diagram of this is shown in Figure 2 (Maitland 1986). A PPIVM of the lumbar spine revealed limitation of the L3±L5 extension, supporting the observation and palpation ®ndings (Maitland 1986). Re-testing Rotation of the left foot in the air (the patient's marker) was tested before and after the palpation of the lumbar spine. This was re-tested after each physical test and no change in symptoms was found except after the palpation of the lumbar spine. She found that the foot was less sti and slightly less painful after this procedure. This was a surprise for the patient, who had expressed diculty in understanding why the lumbar spine should be investigated when she had been diagnosed with a sprained ankle. She expressed how sure she was that her injury was a purely local problem. The rationale for the chosen treatment It was concluded that neural tissue was most likely to be responsible for her symptoms, mainly because of the increase in symptoms with cervical spine ¯exion on the SLR with inversion test. It was hypothesized that the stiness of her lumbar spine was related to the alteration of her neural supply to her left lower leg, as the nerves in the involved area originate from
Resisted movements, foot and ankle Resisted movements testing the muscles and tendons of the ankle were all unremarkable. Palpation of the Achilles tendon and the sural nerve To investigate local structures as possible paincausing structures, the Achilles tendon and the scar tissue resulting from the tear were palpated. This was pain free. On palpation of the sural nerve, only vague discomfort was elicited and the pain she complained of was not reproduced. # 1999 Harcourt Publishers Ltd
Fig. 2ÐMovement diagram of L5 perceived resistance related to the pain feed-back; R represents resistance: R1 onset of resistance; R0 was equivalent to a grade IV. P represents pain; P1 is onset of pain; P2 was equivalent to 4/10. L represents the limit to the movement, in this case limited by pain. Manual Therapy (1999) 4(3), 163±168
166 Manual Therapy
the L4 to the S3 nerve roots. Her L5 transverse process was sore, had restricted movements on palpation and, as her symptoms improved after the lumbar spine palpation, a similar mobilization was used as the ®rst choice of treatment. The increase of dorsi¯exion of the left ankle found in the lunge test probably re¯ected how the tendon had healed following the tear. A double crush sydrome (Butler 1991) could have occurred as a result of the scar tissue following the healing of the Achilles tendon tear. Such scar tissue could have caused compression of the dorsal lateral cutaneous branch of the sural nerve. This compression was hypothesized to be part of the possible pathology responsible for the patient's complaint. The site of a distal compression will easily become in¯amed leading to changes in conduction and possible pain responses (Butler 1991). The successful recovery is dependent on treatment at all interfaces where the axoplasmic ¯ow is impaired. Signs and symptoms were improved after lumbar palpation and it was hypothesized that an increase in axoplasmic ¯ow could be a possible explanation. The treatment provided A left unilateral mobilization grade III (Maitland 1986) was applied at the L5 transverse process and repeated 3 times for 30 seconds each. The patient experienced a slight local pain with the rhythm. On re-testing of the left SLR with inversion, and on sitting rotating the foot in the air was symptom-free in both cases. At her next consultation, 1 week later, she had been symptom-free except for a few occasions while walking. On SLR with inversion and on circling the foot in the air she experienced slight pain. The treatment from the previous week was repeated again with the result that the complaints disappeared on re-testing. She was instructed in auto-mobilizing exercises for her lumbar spine, which consisted of extension exercises in supine, with the emphasis on movement located around the L5 level. She was furthermore instructed in balancing exercises, standing on one leg to increase strength and proprioception of the leg, as she expressed that she did not trust that her leg and foot would be strong enough for a tennis game, as a result of the injury. Grieve (1988) argued that sensory and motor function of a nerve is likely to be somewhat aected when the nerve conduction is impaired, which could be part of the explanation for her lack of trust in her leg. At her third visit she was free of any complaints, felt `much stronger, and had a better awareness of her leg' than she had felt before the onset of pain in her ankle. She was also very pleased with the fact that she could understand the reasoning behind the reoccurrence of symptoms in the left leg. Manual Therapy (1999) 4(3), 163±168
EVALUATION OF THE TREATMENT PROVIDED Re¯ective analysis of the rapid improvement of this patient's symptoms indicates that the cause of the symptoms could possibly have been a reversible restriction of the conduction of a nerve root structure. A nerve stops conducting when its oxygen supply is deprived. An increase in pressure on the nerve, e.g. from oedema, may cause pressure on the blood vessels within the nerve, causing an occlusion of these and leading to a lack of oxygen supply to the nerve. The nerve may however maintain sub-optimal conduction ability as oxygen may be supplied via diusion. This diusion occurs via the axoplasmic ¯ow: this may continuously ¯ow in the partiallycompressed nerve. As soon as the oedema that causes the compression is relieved, a spontaneous return to normal conduction can be seen. A demand for successful conduction recovery after a decreased oxygen supply is that the axons and blood vessels are not damaged (Grieve 1988). The neurological tests did not reveal any decreased nerve conduction. To support the hypothesis of altered nerve conduction presented in this study, further nerve conduction tests such as vibration tests as described by Greening and Lynn (1998b) could have been performed. These tests are argued to be more sensitive to changes in nerve conduction than the tests used in this study (Greening & Lynn 1998b). The outcome of the treatment indicated that neural pain related to poor conduction could be present without any changes in nerve conduction tests. Although vibration tests may be more sensitive, it may not be able to measure conduction changes reliably despite pain related to nerve dysfunction. The patient reported that she felt her symptoms had improved by 90% before the treatment was commenced and it would therefore be hypothesized that the patient was improving and would have achieved full recovery, even if no treatment had been provided. Some factors, however, indicate that the treatment made a signi®cant dierence. Firstly, that the symptoms were not provoked while re-testing after the treatment. Secondly, she reported that the leg felt much stronger and that she had a better awareness of the leg than before the pain had started 4 weeks prior to the ®rst physiotherapy consultation. At her second consultation, she was instructed to perform balance exercises and at her third and last visit, she had performed these exercises for 1 week. It is unlikely that 1 week of balancing exercises alone would cause such a signi®cant change in the strength and awareness of the leg. When connective tissue is stretched, e.g. during a mobilization, ¯uid is forced out of the tissue. The excessive ¯uid, e.g. due to any oedema contained in # 1999 Harcourt Publishers Ltd
Case report 167
connective tissue, may therefore by hypothesized to have been aided in escaping from this tissue during a repeated unilateral mobilization (Giord 1994). Oedema in the nerve root canal may be of signi®cant importance as the peripheral nerve is especially susceptible to compression here (Shacklock et al. 1994). The spine was found sti on palpation and it could be hypothesized that a decrease of intervertebral movement could impair the conduction of the nerve. Movement of the spine is thought to increase the nutrition and removal of waste products from the nerve and thereby help relieve the symptoms arguably caused by oedema, compressing the nerve. The axoplasmic ¯ow of the nerve may in particular have been helped by the accessory mobilization provided, as movement of the spine is thought to improve the ¯ow characteristics of the axoplasm and make this thinner (Shacklock et al. 1994). The accessory movement may have caused movement that could not normally be produced by the patient and therefore caused the rapid improvement of symptoms. Stiness of joints can be due to previous in¯ammation. Acute in¯ammation causes joint stiness (Giord 1994) and the collagen formed in the repair process may lead to tissue stiness (Evans 1980). Mobilizing the sti intervertebral joint may therefore lead to recovery of a nerve root pathology as improvement of joint movements will enable the joint to `keep up' with the movement of the nervous system at the intersegmental level (Shacklock et al. 1994). This patient did not present with a history of lower back pain and it could be hypothesized that the stiness presented was congenital. The stiness, related to previous in¯ammation or congenital stiness, could provide at least part of the explanation of the decreased muscle bulk of the calf muscle, presented during her pregnancies. An intervertebral canal related to an intervertebral joint with limited movement will have a tendency of decrease ¯uid transport in the canal because of the stiness. During pregnancy, plasma volume increases with a tendency to ¯uid retention (Verkeste et al. 1998), consequently the amount of ¯uid in the intervertebral canal could increase, thereby increasing the pressure in the canal. This increase could lead to compression of the nerve root, which may lead to decreased nerve conduction. As this particular joint seems to present with limited movement, it would be particularly likely that ¯uid transport would be limited. These factors could lead to the decrease in muscle bulk presented during her pregnancies and may be a more realistic explanation for the decrease than the one presented by the patient's previous physiotherapist. The repeated compression of the nerve root during her three pregnancies could be argued to have caused ®bre deformation (Grieve 1988) and therefore leave # 1999 Harcourt Publishers Ltd
the nerve more susceptible to a reaction from nerve root compression. Rapid recovery of signs and symptoms has, in other case reports (Wilson 1997; Zvulun 1998), been hypothesized to be related to recovery of impaired nerve conduction. The ®ndings in these reports concur with the conclusion of this study: treatment aimed at improving the neural conduction is capable of helping the recovery of peripheral pathology. Greening and Lynn (1998a) discussed that both compression and in¯ammation of a nerve could cause a decrease in the conduction of the nerve. The rapid recovery of the nerve conduction found in this study indicates that the causal factor for the decreased conduction was compression, rather than in¯ammation. An in¯ammation process lasts several days (Evans 1980) and would therefore not be altered in a matter of minutes. In¯ammation would furthermore often provoke local pain, which was not seen in the above-mentioned cases. The manual treatment provided may have altered the oxygen supply (Grieve 1988) and/or helped the quality of the axoplasmic ¯ow (Shacklock et al 1994). Zvulum (1998) found that using mobilizing techniques of the nerves helped to resolve impaired nerve conduction. Such techniques could have been utilized if the approach chosen had been insucient. The scar tissue following the healing of the tear could impair movement of the nerve and thereby the axoplasmic ¯ow locally at the sural nerve. A nerve mobilization would have been particularly helpful for improving the nerve movement at such an interface. The unilateral mobilization could have been performed in lumbar extension, as this was the movement that was found sti. This could have been an alternative treatment technique if the treatment provided had not been sucient for the recovery of the patient's signs and symptoms. CONCLUSION The pathology of a peripheral nerve might be caused by impairment of the axoplasmic ¯ow within the nerve. Impairment of this ¯ow might also cause pathology of somatic structures innervated by the nerve involved. The relevant neural tissue should be assessed in all patients presenting with peripheral complaints. This is especially indicated when the history indicates a possible involvement of neural tissue. Assessment of conduction alteration and/or mobility of the nerve system may give an indication whether neural pathology is causing the patients complaint. The rationale behind treating injuries in the lower extremities, using techniques applied at the lower back, might be dicult for the patient to comprehend. Good communication skills are important for Manual Therapy (1999) 4(3), 163±168
168 Manual Therapy
the patient's understanding of the relevance of treatment. Lumbar spine stiness may have an in¯uence on the conduction of a nerve. Stiness may be present in a joint, which repeatedly has been subjected to an in¯ammatory process or may be congenital in nature. Manual therapy to the lower back might lead to rapid improvement of nerve conduction, leading to a fast resolution of a pathological condition in the lower extremities. It is a suggestion of this case report that altered nerve conduction might occur without in¯ammation of the nerve. Acknowledgement The author would like to thank Julie Stenning, David Brook®eld and Claudia Gin for constructive comments and generous help with proof reading. References Butler DS 1991 Mobilisation of the Nervous System. Churchill Livingstone, Melbourne Evans P 1980 The healing process at cellular level: a review. Physiotherapy 66(8): 256±259 Giord LS 1994 In¯uence of circadian variation on spinal examination. In: Boyling JD, Palastanga N (eds) Grieve's Modern Manual Therapy: The Vertebral Column. Churchill Livingstone, Edinburgh, pp 503±509
Manual Therapy (1999) 4(3), 163±168
Greening J, Lynn B 1998a Minor peripheral nerve injuries: an underestimated source of pain? Manual Therapy 3(4): 187±194 Greening J, Lynn B 1998b Vibration sense in the upper limb in patients with repetitive strain injury and a group of at risk oce workers. International Archives of Occupational and Environmental Medicine 71: 29±34 Grieve GP 1988 Common Vertebral Joint Problems. Churchill Livingstone, Edinburgh Kaltenborn FM 1989 Manual Mobilization of the Extremity Joints: Basic Examination and Treatment, 4th Edition. Olaf Norlis Bokhandel, Oslo Maitland GD 1986 Vertebral Manipulation, 5th Edition. Butterworth±Heinemann, London Maitland GD 1991 Peripheral Manipulation, 3rd Edition. Butterworth±Heinemann, London Mandelbaum BR, Myerson MS, Forster R 1995 Achilles tendon ruptures. A new method of repair, early range of motion, and functional rehabilitation. The American Journal of Sports Medicine 23(4): 392±395 Sandler SE 1996 The management of low back pain in pregnancy. Manual Therapy 1(4): 178±185 Scott J, Huskisson EC 1979 Vertical and horizontal visual analogue scales. Annals of the Rheumatic Diseases 38: 560 Shacklock MO, Butler DS Slater H 1994 The dynamic central nervous system: structure and clinical neurobiomechanics. In: Boyling JD, Palastanga N (eds) Grieve's Modern Manual Therapy: The Vertebral Column. Churchill Livingstone, Edinburgh, pp 21±38 Verkeste CM, Slangen BF, Dubelaar ML, van-Kreel BK, Peeters LL 1998 Mechanism of volume adaptation in the awake early pregnant rat. American Journal of Physiology 5: 274±279 Wilson E 1997 Central facilitation and remote eects: treating both ends of the system. Manual Therapy 2(2): 165±168 Zvulun I 1998 Mobilizing the nervous system in cervical cord compression. Manual Therapy 3(1): 42±47
# 1999 Harcourt Publishers Ltd
Case report
The case of a non-traumatic sprained ankle C. Uth School of Healthcare Professions, University of Brighton, Sussex, UK
alteration of the sensory and motor functioning of the target tissues. An alteration of the axoplasmic ¯ow has further importance in terms of the nutrition of the nerve and if the ¯ow is diminished, it will leave the peripheral part of the nerve vulnerable and prone to injury (Butler 1991). Furthermore, Butler (1991) suggested that a restriction of the axoplasmic ¯ow might cause trophic changes in the target tissues such as muscle and skin, causing damage to cell bodies and the axon. He suggested that this damage could be a possible explanation for injuries such as an Achilles tendon tear or lateral epicondylitis. In¯ammation of a nerve may lead to an irritation of the free nerve endings of the nervi nervorum (Greening & Lynn 1998a). The pain sensation from an in¯amed nerve is often described as causing bizarre or unfamiliar symptoms, examples are a burning or a crawling sensation (Butler 1991). Laminar nerve root compression is a common consequence to spondylolisthesis (Grieve 1988). Nerve root compression may also be due to an in¯ammation of extra neural soft tissue such as intervertebral disc, fat tissue, ligaments and joint capsules causing pressure on the nerve (Butler 1991).
INTRODUCTION Signs and symptoms originating from the nervous system may be far more common than we are aware of in our daily clinical work. Compression of a peripheral nerve can lead to neuropathy causing alterations in sensation and/or strength in areas distant to the location of the injury or to a neuropathy, with pain as the response from the peripheral nerve system (Butler 1991). Compression is most likely to happen in areas where there is limited room for oedema to escape or where mechanical pressure directly compresses the nerve at the soft tissue and/or bony interfaces (Butler 1991). A local distal neuropathy may be particularly aggravated when a provocation is directly applied to the area, yet the cause of the symptoms might be a compression located more centrally, e.g. at the root of a peripheral nerve. This can easily lead to a confusion as to which structure is causing the symptoms. The successful rehabilitation will, in cases like these, depend on the treatment of the underlying pathology, for example at the nerve root. Long-standing compression of a peripheral nerve does not necessarily cause clinical changes, such as an alteration in sensation and/or a decrease in muscle power (Grieve 1988), and a nerve root compression alone is not painful (Grieve 1988). A nerve can withstand severe compression without changes in conduction or pain response. Greening and Lynn (1998a) argued that both in¯ammation and compression of a nerve root could cause decreased nerve conduction. Chronic compression is thought to be a source of nerve root in¯ammation and an in¯ammatory process causes changes such as local ischaemia, oedema, ®bre deformation, entrapment and ®brosis (Grieve 1988). The ®brosis, as well as the oedema, restricts the axoplasmic ¯ow, which is important for the conduction of the nerve. This may lead to an
SUBJECTIVE EXAMINATION The patient concerned in this case report was a 38year-old woman, diagnosed by her General Practitione (GP) with a ``sprained ankle''. She presented herself for treatment with symptoms, which had started 4 weeks prior to the physiotherapy consultation. The onset of the symptoms began whilst walking; she experienced a sudden sharp, unprovoked pain at the lateral side of her left ankle, which she rated as being 6 out of 10 on a visual analogue scale (VAS) (Scott & Huskisson 1979). She consulted her GP on two occasions over the following 4 weeks, complaining of lateral ankle pain. This swelling was diagnosed as a sprained ankle and she was told that her symptoms would heal within a couple of weeks.
Carsten Uth, DipPhty (Den.), MCSP, 10 Walcot Court, 1B Ashburton Road, Croydon CR0 6AP, UK. 163
164 Manual Therapy
This diagnosis was given in spite of the fact that she had not experienced any twisting of her ankle. As the ankle had not improved satisfactorily after almost 4 weeks, she contacted our physiotherapy clinic. Over the previous 4 weeks, she had been able to play tennis with low intensity on two occasions, experiencing some left ankle pain. Wearing an ankle support eased this. The swelling had decreased by 90% over the previous couple of days and as her GP had told her that her ankle would recover by itself, she almost felt ashamed to seek help, despite stiness and some pain in the ankle. At her ®rst visit to the clinic, her main complaint was stiness of the left ankle, a dull ache, which she rated as 0.5 out of 10 on a VAS and that the foot did not `feel right' (Fig. 1.) Pain was aggravated when depressing the clutch of her car and this decreased as soon as the clutch was released. In sitting, circling her left foot in the air produced the stiness and pain she complained of in her left ankle. This function was chosen as a subjective marker. During walking, sitting and standing she was free of pain. Her previous medical history included an injury to the left lower leg and proved to be of relevance to the current problem. Approximately 10 years ago she had experienced an almost complete tear of her left Achilles tendon at the end of a recreational tennis game. This was treated with 5 weeks in plaster followed by physiotherapy rehabilitation over a 3 week period. She had since had three children and with each pregnancy, she had experienced clear atrophy of her left triceps surae muscles. She could not recall any severe lower back pain. She had received physiotherapy treatment for this muscle
wasting at another physiotherapy clinic and it had been explained to her that the hormones released during pregnancy, to enable the birth passage to increase, were responsible for the weakening of her ligaments. She was told that this hormone release was also responsible for the weakening of her left Achilles tendon, thereby causing muscle weakness of the left calf muscle. She was rehabilitated with strengthening exercises and recovered fully after each birth. Special questions (Maitland 1986) only revealed a tendency to epilepsy for which she took one mild epilepsy tablet on a daily basis. During the previous 10 years, she had only experienced four mild attacks.
INITIAL IMPRESSION AFTER THE SUBJECTIVE EXAMINATION The initial impression following the subjective questioning indicated that signs and symptoms of her presentation did not ®t together. She complained of lateral ankle pain, which her GP had diagnosed to be a twisted ankle. The structures of the ankle would have to be investigated, but lack of injury to the local area suggested that more central ± neural structures would have to be investigated too. Tearing of the Achilles tendon had happened 10 years ago, which meant that she would have been 28-years-old at the time. Mandelbaum et al. (1995) referred to reports showing that 75% of Achilles tendon injuries occur in athletes, predominantly men between 30 and 40 years of age. A rupture at the age of 28 in a female might therefore be an unusual phenomenon and could possibly be linked to Butler's suggestions (1991) that altered axoplasmic ¯ow creating trophic changes in muscles and tendons may cause tears like these. The patient's muscle atrophy of her left calf muscle during her three pregnancies could furthermore indicate altered nerve conduction. A thorough assessment of her lower back and neural structures was indicated. Her previous physiotherapists had suggested that her calf muscle atrophy could be linked to the release of hormones ± this explanation was found to lack support. If the wasting was related to hormones, such symptoms would have been more widespread in the body (Sandler 1996).
PHYSICAL EXAMINATION Observation
Fig. 1ÐBody chart with the distribution of pain. Manual Therapy (1999) 4(3), 163±168
It was noted that the patient had a ¯attish spine, a slight right convex scoliosis in the thorax area, decreased left calf muscle bulk and a thickened left Achilles tendon with postoperative scar tissue at the lateral part of the tendon. In general, she was tall and thin with a tiny physique; an ectomorph. # 1999 Harcourt Publishers Ltd
Case report 165
Lumbar spine movements Extension appeared restricted by approximately 50% due to stiness. Flexion was unremarkable, as were lateral ¯exion and rotation to each side. Gait Her pain was reproduced when walking on her toes. It was also noted that her scoliosis increased during stance-phase on her left leg during normal gait. Dynamic tests A lunge test indicated that she had approximately 15% increased range of movement in her left ankle dorsi¯exion, with the knee both straight and slightly ¯exed, indicating an increased length of both gastrocnemius and soleus. Neurological tests All sensation, muscle strength and re¯ex tests of the left leg were comparable to the non-involved side. Neurodynamic tests Straight Leg Raise (SLR) was, on both legs, restricted by resistance at approximately 60 degrees and produced no symptoms. When her left ankle was inverted to nearly end of range her pain was exactly reproduced. Furthermore, this pain was increased with cervical ¯exion. This was chosen as an additional marker. No pain was produced on inversion of her right foot in SLR. Passive movement tests Physiological dierentiation movements of the ankle and foot indicated that inversion was the aggravating factor. Various tests (Kaltenborn 1989; Maitland 1991) of the ankle and lower leg joints were performed and all individual joints were found normal. The hip and knee joints were all normal too.
Palpation and Passive Physiological intervertebral Movements (PPIVM) of the lumbar spine Passive accessory intervertebral movement examination of her lumbar spine showed that her lumbar spine was very sti on unilateral palpation bilaterally over the facet joints from the L3 to L5. Furthermore, pain was elicited on unilateral pressure applied to her left L5 transverse process. The movement diagram of this is shown in Figure 2 (Maitland 1986). A PPIVM of the lumbar spine revealed limitation of the L3±L5 extension, supporting the observation and palpation ®ndings (Maitland 1986). Re-testing Rotation of the left foot in the air (the patient's marker) was tested before and after the palpation of the lumbar spine. This was re-tested after each physical test and no change in symptoms was found except after the palpation of the lumbar spine. She found that the foot was less sti and slightly less painful after this procedure. This was a surprise for the patient, who had expressed diculty in understanding why the lumbar spine should be investigated when she had been diagnosed with a sprained ankle. She expressed how sure she was that her injury was a purely local problem. The rationale for the chosen treatment It was concluded that neural tissue was most likely to be responsible for her symptoms, mainly because of the increase in symptoms with cervical spine ¯exion on the SLR with inversion test. It was hypothesized that the stiness of her lumbar spine was related to the alteration of her neural supply to her left lower leg, as the nerves in the involved area originate from
Resisted movements, foot and ankle Resisted movements testing the muscles and tendons of the ankle were all unremarkable. Palpation of the Achilles tendon and the sural nerve To investigate local structures as possible paincausing structures, the Achilles tendon and the scar tissue resulting from the tear were palpated. This was pain free. On palpation of the sural nerve, only vague discomfort was elicited and the pain she complained of was not reproduced. # 1999 Harcourt Publishers Ltd
Fig. 2ÐMovement diagram of L5 perceived resistance related to the pain feed-back; R represents resistance: R1 onset of resistance; R0 was equivalent to a grade IV. P represents pain; P1 is onset of pain; P2 was equivalent to 4/10. L represents the limit to the movement, in this case limited by pain. Manual Therapy (1999) 4(3), 163±168
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the L4 to the S3 nerve roots. Her L5 transverse process was sore, had restricted movements on palpation and, as her symptoms improved after the lumbar spine palpation, a similar mobilization was used as the ®rst choice of treatment. The increase of dorsi¯exion of the left ankle found in the lunge test probably re¯ected how the tendon had healed following the tear. A double crush sydrome (Butler 1991) could have occurred as a result of the scar tissue following the healing of the Achilles tendon tear. Such scar tissue could have caused compression of the dorsal lateral cutaneous branch of the sural nerve. This compression was hypothesized to be part of the possible pathology responsible for the patient's complaint. The site of a distal compression will easily become in¯amed leading to changes in conduction and possible pain responses (Butler 1991). The successful recovery is dependent on treatment at all interfaces where the axoplasmic ¯ow is impaired. Signs and symptoms were improved after lumbar palpation and it was hypothesized that an increase in axoplasmic ¯ow could be a possible explanation. The treatment provided A left unilateral mobilization grade III (Maitland 1986) was applied at the L5 transverse process and repeated 3 times for 30 seconds each. The patient experienced a slight local pain with the rhythm. On re-testing of the left SLR with inversion, and on sitting rotating the foot in the air was symptom-free in both cases. At her next consultation, 1 week later, she had been symptom-free except for a few occasions while walking. On SLR with inversion and on circling the foot in the air she experienced slight pain. The treatment from the previous week was repeated again with the result that the complaints disappeared on re-testing. She was instructed in auto-mobilizing exercises for her lumbar spine, which consisted of extension exercises in supine, with the emphasis on movement located around the L5 level. She was furthermore instructed in balancing exercises, standing on one leg to increase strength and proprioception of the leg, as she expressed that she did not trust that her leg and foot would be strong enough for a tennis game, as a result of the injury. Grieve (1988) argued that sensory and motor function of a nerve is likely to be somewhat aected when the nerve conduction is impaired, which could be part of the explanation for her lack of trust in her leg. At her third visit she was free of any complaints, felt `much stronger, and had a better awareness of her leg' than she had felt before the onset of pain in her ankle. She was also very pleased with the fact that she could understand the reasoning behind the reoccurrence of symptoms in the left leg. Manual Therapy (1999) 4(3), 163±168
EVALUATION OF THE TREATMENT PROVIDED Re¯ective analysis of the rapid improvement of this patient's symptoms indicates that the cause of the symptoms could possibly have been a reversible restriction of the conduction of a nerve root structure. A nerve stops conducting when its oxygen supply is deprived. An increase in pressure on the nerve, e.g. from oedema, may cause pressure on the blood vessels within the nerve, causing an occlusion of these and leading to a lack of oxygen supply to the nerve. The nerve may however maintain sub-optimal conduction ability as oxygen may be supplied via diusion. This diusion occurs via the axoplasmic ¯ow: this may continuously ¯ow in the partiallycompressed nerve. As soon as the oedema that causes the compression is relieved, a spontaneous return to normal conduction can be seen. A demand for successful conduction recovery after a decreased oxygen supply is that the axons and blood vessels are not damaged (Grieve 1988). The neurological tests did not reveal any decreased nerve conduction. To support the hypothesis of altered nerve conduction presented in this study, further nerve conduction tests such as vibration tests as described by Greening and Lynn (1998b) could have been performed. These tests are argued to be more sensitive to changes in nerve conduction than the tests used in this study (Greening & Lynn 1998b). The outcome of the treatment indicated that neural pain related to poor conduction could be present without any changes in nerve conduction tests. Although vibration tests may be more sensitive, it may not be able to measure conduction changes reliably despite pain related to nerve dysfunction. The patient reported that she felt her symptoms had improved by 90% before the treatment was commenced and it would therefore be hypothesized that the patient was improving and would have achieved full recovery, even if no treatment had been provided. Some factors, however, indicate that the treatment made a signi®cant dierence. Firstly, that the symptoms were not provoked while re-testing after the treatment. Secondly, she reported that the leg felt much stronger and that she had a better awareness of the leg than before the pain had started 4 weeks prior to the ®rst physiotherapy consultation. At her second consultation, she was instructed to perform balance exercises and at her third and last visit, she had performed these exercises for 1 week. It is unlikely that 1 week of balancing exercises alone would cause such a signi®cant change in the strength and awareness of the leg. When connective tissue is stretched, e.g. during a mobilization, ¯uid is forced out of the tissue. The excessive ¯uid, e.g. due to any oedema contained in # 1999 Harcourt Publishers Ltd
Case report 167
connective tissue, may therefore by hypothesized to have been aided in escaping from this tissue during a repeated unilateral mobilization (Giord 1994). Oedema in the nerve root canal may be of signi®cant importance as the peripheral nerve is especially susceptible to compression here (Shacklock et al. 1994). The spine was found sti on palpation and it could be hypothesized that a decrease of intervertebral movement could impair the conduction of the nerve. Movement of the spine is thought to increase the nutrition and removal of waste products from the nerve and thereby help relieve the symptoms arguably caused by oedema, compressing the nerve. The axoplasmic ¯ow of the nerve may in particular have been helped by the accessory mobilization provided, as movement of the spine is thought to improve the ¯ow characteristics of the axoplasm and make this thinner (Shacklock et al. 1994). The accessory movement may have caused movement that could not normally be produced by the patient and therefore caused the rapid improvement of symptoms. Stiness of joints can be due to previous in¯ammation. Acute in¯ammation causes joint stiness (Giord 1994) and the collagen formed in the repair process may lead to tissue stiness (Evans 1980). Mobilizing the sti intervertebral joint may therefore lead to recovery of a nerve root pathology as improvement of joint movements will enable the joint to `keep up' with the movement of the nervous system at the intersegmental level (Shacklock et al. 1994). This patient did not present with a history of lower back pain and it could be hypothesized that the stiness presented was congenital. The stiness, related to previous in¯ammation or congenital stiness, could provide at least part of the explanation of the decreased muscle bulk of the calf muscle, presented during her pregnancies. An intervertebral canal related to an intervertebral joint with limited movement will have a tendency of decrease ¯uid transport in the canal because of the stiness. During pregnancy, plasma volume increases with a tendency to ¯uid retention (Verkeste et al. 1998), consequently the amount of ¯uid in the intervertebral canal could increase, thereby increasing the pressure in the canal. This increase could lead to compression of the nerve root, which may lead to decreased nerve conduction. As this particular joint seems to present with limited movement, it would be particularly likely that ¯uid transport would be limited. These factors could lead to the decrease in muscle bulk presented during her pregnancies and may be a more realistic explanation for the decrease than the one presented by the patient's previous physiotherapist. The repeated compression of the nerve root during her three pregnancies could be argued to have caused ®bre deformation (Grieve 1988) and therefore leave # 1999 Harcourt Publishers Ltd
the nerve more susceptible to a reaction from nerve root compression. Rapid recovery of signs and symptoms has, in other case reports (Wilson 1997; Zvulun 1998), been hypothesized to be related to recovery of impaired nerve conduction. The ®ndings in these reports concur with the conclusion of this study: treatment aimed at improving the neural conduction is capable of helping the recovery of peripheral pathology. Greening and Lynn (1998a) discussed that both compression and in¯ammation of a nerve could cause a decrease in the conduction of the nerve. The rapid recovery of the nerve conduction found in this study indicates that the causal factor for the decreased conduction was compression, rather than in¯ammation. An in¯ammation process lasts several days (Evans 1980) and would therefore not be altered in a matter of minutes. In¯ammation would furthermore often provoke local pain, which was not seen in the above-mentioned cases. The manual treatment provided may have altered the oxygen supply (Grieve 1988) and/or helped the quality of the axoplasmic ¯ow (Shacklock et al 1994). Zvulum (1998) found that using mobilizing techniques of the nerves helped to resolve impaired nerve conduction. Such techniques could have been utilized if the approach chosen had been insucient. The scar tissue following the healing of the tear could impair movement of the nerve and thereby the axoplasmic ¯ow locally at the sural nerve. A nerve mobilization would have been particularly helpful for improving the nerve movement at such an interface. The unilateral mobilization could have been performed in lumbar extension, as this was the movement that was found sti. This could have been an alternative treatment technique if the treatment provided had not been sucient for the recovery of the patient's signs and symptoms. CONCLUSION The pathology of a peripheral nerve might be caused by impairment of the axoplasmic ¯ow within the nerve. Impairment of this ¯ow might also cause pathology of somatic structures innervated by the nerve involved. The relevant neural tissue should be assessed in all patients presenting with peripheral complaints. This is especially indicated when the history indicates a possible involvement of neural tissue. Assessment of conduction alteration and/or mobility of the nerve system may give an indication whether neural pathology is causing the patients complaint. The rationale behind treating injuries in the lower extremities, using techniques applied at the lower back, might be dicult for the patient to comprehend. Good communication skills are important for Manual Therapy (1999) 4(3), 163±168
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the patient's understanding of the relevance of treatment. Lumbar spine stiness may have an in¯uence on the conduction of a nerve. Stiness may be present in a joint, which repeatedly has been subjected to an in¯ammatory process or may be congenital in nature. Manual therapy to the lower back might lead to rapid improvement of nerve conduction, leading to a fast resolution of a pathological condition in the lower extremities. It is a suggestion of this case report that altered nerve conduction might occur without in¯ammation of the nerve. Acknowledgement The author would like to thank Julie Stenning, David Brook®eld and Claudia Gin for constructive comments and generous help with proof reading. References Butler DS 1991 Mobilisation of the Nervous System. Churchill Livingstone, Melbourne Evans P 1980 The healing process at cellular level: a review. Physiotherapy 66(8): 256±259 Giord LS 1994 In¯uence of circadian variation on spinal examination. In: Boyling JD, Palastanga N (eds) Grieve's Modern Manual Therapy: The Vertebral Column. Churchill Livingstone, Edinburgh, pp 503±509
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Greening J, Lynn B 1998a Minor peripheral nerve injuries: an underestimated source of pain? Manual Therapy 3(4): 187±194 Greening J, Lynn B 1998b Vibration sense in the upper limb in patients with repetitive strain injury and a group of at risk oce workers. International Archives of Occupational and Environmental Medicine 71: 29±34 Grieve GP 1988 Common Vertebral Joint Problems. Churchill Livingstone, Edinburgh Kaltenborn FM 1989 Manual Mobilization of the Extremity Joints: Basic Examination and Treatment, 4th Edition. Olaf Norlis Bokhandel, Oslo Maitland GD 1986 Vertebral Manipulation, 5th Edition. Butterworth±Heinemann, London Maitland GD 1991 Peripheral Manipulation, 3rd Edition. Butterworth±Heinemann, London Mandelbaum BR, Myerson MS, Forster R 1995 Achilles tendon ruptures. A new method of repair, early range of motion, and functional rehabilitation. The American Journal of Sports Medicine 23(4): 392±395 Sandler SE 1996 The management of low back pain in pregnancy. Manual Therapy 1(4): 178±185 Scott J, Huskisson EC 1979 Vertical and horizontal visual analogue scales. Annals of the Rheumatic Diseases 38: 560 Shacklock MO, Butler DS Slater H 1994 The dynamic central nervous system: structure and clinical neurobiomechanics. In: Boyling JD, Palastanga N (eds) Grieve's Modern Manual Therapy: The Vertebral Column. Churchill Livingstone, Edinburgh, pp 21±38 Verkeste CM, Slangen BF, Dubelaar ML, van-Kreel BK, Peeters LL 1998 Mechanism of volume adaptation in the awake early pregnant rat. American Journal of Physiology 5: 274±279 Wilson E 1997 Central facilitation and remote eects: treating both ends of the system. Manual Therapy 2(2): 165±168 Zvulun I 1998 Mobilizing the nervous system in cervical cord compression. Manual Therapy 3(1): 42±47
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