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CASE REPORT
Sudden Onset Foot Drop From Peroneal Ganglia
*Rajinder Singh Gaheer,  +Jamie Mckenzie, ** Maurice Paterson

* Registrar, Department of Orthopaedics, Dumfries and Galloway Royal Infirmary, Dumfries, United Kingdom, DG1 4AP
+ Specialist Registrar, Department of Orthopaedics, Royal United Hospital Bath NHS Trust, Bath, United Kingdom, BA1 3NG.
**Consultant, Department of Orthopaedics, Royal United Hospital Bath NHS Trust, Bath, United Kingdom, BA1 3NG.

Address for Correspondence

Mr Rajinder Singh Gaheer
10 Maryfield Terrace, Dumfries, United Kingdom, DG1 4UG
Phone: 00(44)1387246246 Ext. 2001
Fax: 00(44)1387241193
Email: rsgaheer@hotmail.com

Abstract

Sudden onset loss of ankle dorsiflexion is rarely caused by compression of the common peroneal nerve by ganglion cysts. Peroneal nerve ganglion cysts typically present with a palpable mass or features of entrapment neuropathy, including pain, gradual onset motor and sensory weakness.
Ganglion cysts are common in upper extremity, most often occurring in the wrist.1 They are relatively uncommon in the lower extremity, most commonly involving the peroneal nerve.2   Involvement of the nerve commonly occurs by compression by these cysts originating from a neighbouring joint. Compression neuropathy of the peroneal nerve most commonly presents with pain along its distribution and in most cases identifiable swelling or mass at the proximal fibula. For this reason sensory loss or motor weakness is relatively uncommon. When this occurs, it is gradual and develops over the course of a period of time because of gradual extrinsic compression of the nerve. The cases reported here are of two instances of ganglion cysts arising from the proximal tibiofibular joint where there was sudden onset of foot drop. No prior weakness or sensory symptoms were noted and an identifiable swelling was not reported by the patient. In both instances lumbar disc disease was thought to be the cause of footdrop at initial assessment.
Keywords: peroneal nerve, proximal tibiofibular joint, ganglion cyst, footdrop

J.Orthopaedics 2006;3(4)e20

Introduction:

We report two cases of sudden onset of footdrop due to ganglion cyst arising from the proximal tibiofibular joint. Magnetic Resonance Imaging was used to confirm the diagnosis. Both were successfully treated by excision of the ganglion cyst.

 

Case reports

CASE 1
A 67-year-old lady presented to her GP with sudden onset of right-sided foot drop.  She had mild pre-existing back symptoms but no shooting pain down the leg. There was no history of trauma. She was referred by her GP to our hospital. On examination, there was some wasting of the lateral compartment of the leg. She had reduced sensation over dorsum of foot distally and less so extending into the front of the shin. There was Grade 2 power of invertors, evertors, ankle dorsiflexors and EHL. Plantar flexion was grade 4. Examination of back and hip was normal. Knee examination was unremarkable as well and movements were reasonably good with some mild effusion and mild patello femoral crepitus. Peripheral pulses were intact. Tinel tap was positive at proximal end of fibula.

X-ray of the knee was normal. MRI showed a large well demarcated soft tissue swelling arising from the proximal tibiofibular joint, (Fig- 1,2). The swelling was homogenous and had a hypointense signal on T1-weighted images and hyperintense on T2-weighted images. There was no destruction of the surrounding bony components. This was causing a visible compression of the peroneal nerve.
Surgical exploration and excision of the cystic mass was done nearly 9 months after the first symptoms. It was found to be a large cystic mass communicating with the proximal tibiofubular joint, (Fig- 3). The nerve was found visibly scarred at the time of surgery from the pressure of the cyst. Microscopic examination revealed the mass to be a ganglion cyst.

Within two months of the surgery there was improvement in sensory symptoms. Foot was no longer in inverted position but was neutral.  There was however no active dorsiflexion yet.
Five months after surgery first flicker of dorsiflexion and eversion was noticed.  There was still some paraesthesia in the toes. Tinel sign was now in the lower third of the leg.
Nine months later, she was making steady progress.  Had grade 3 power of her EHL and EDL and peronei were functioning well at 3+, which were absent previously. She still had some sensory hypoesthesia in her first cleft. Tinel was now at the ankle.
One year after surgery, there was some altered light sensation in the foot with very slight weakness of ankle dorsiflexion. She was able to walk at least one mile without the AFO and cycle two to three miles without discomfort. Was not on any regular analgesia and did not use a stick. She did find coming downstairs difficult but no problems arising from chair.
When last seen in the clinic at two and half years, she was managing to live her life without too much difficulty though she cannot walk at speed. She also found that the leg gets a bit more tired than normal and occasionally aches at night. Repeat MRI showed osteoarthritis with some early cyst formation in the knee but no evidence of recurrence in the region of the proximal tibiofibular joint.

CASE 2
A 48 year old teacher was referred by her GP for complaints of weakness in the lower left leg with some paraesthesia in the lateral lower leg, severe left hip/ upper buttock pain and lower back pain.
he first problem to develop was paraesthesia, which he noticed while playing golf about a year ago. Left groin and buttock pain developed over the same period. Back pain developed later during the course of next six months. Pain was aggravated by getting from sitting to standing, walking, stair use and sudden movements. He had no morning stiffness. He found driving was difficult. There were occasional night pains. About three months ago he suddenly developed weakness in the left lower leg.
On examination he had tenderness at L3- L5 levels with tight spasm in the left erector spinae. Neurologically there was complete foot drop and L4-S1 myotomes were weak. There was no power at all in EDC, evertors or ankle dorsiflexors. His reflexes were normal but he had numbness in the outer border of the calf and foot.
MRI showed a small left-sided L5-S1 disc, which was causing some impression on the S1 nerve root. This however would not explain the dense weakness that he had in the foot.
On further examination he had a palpable lesion around the lateral side of the knee, around the proximal end of fibula.
peroneal nerve or running alongside it. The report indicated that it did not look like a ganglion coming from the knee joint pushing on the nerve and that it would be remarkably long for it to be a schwanomma.
Exploration was done and a cystic mass coming from the proximal tibiofibular joint was identified. This had insinuated its way into the common peroneal nerve and then intraneurally within the fascicles about 5 inches upwards within the common peroneal nerve. Biopsy confirmed that it was an intraneural ganglion.
When last seen in the clinic at a year from surgery he still had some altered sensation in the distribution of the deep and superficial peroneal nerves. He had Grade 4 ankle dorsiflexion and was able to extend all his toes.

Discussion :

Ganglion cysts rarely involve peripheral nerves. They are easily overlooked as potential causes of neuropathy during evaluation of clinical cases of nerve palsy. Ganglion cysts compressing the peroneal nerve can either originate from the proximal tibiofibular joint causing nerve dysfunction secondary to compression, they may also arise by cystic degeneration of the nerve sheath and invade the nerve appearing as intraneural ganglions. Regardless of their origin, these have the potential of growing alongside and invading nerve and thus delay in diagnosis can result in irreversible nerve damage.2 Many hypothesis have been put forward about the pathogenesis of these cysts,3 but the hypothesis of synovial origin from the proximal tibiofibular joint seems most likely.4 This hypothesis enables us to explain the origin of not only extraneural cysts, but also intraneural ones. In effect, in the latter case, the cyst lifts and compresses the nerve, and then produces adherence and fusion between its wall and the nerve sheath.


The cyst from the proximal tibiofibular joint joins the peroneal nerve by means of a small recurrent articular branch.15 Spinner et al 15 stressed the importance of the articular branch and compared the rate of recurrence before and after the surgeons awareness of this branch. Prior to identification of this nerve and failure to address this at operation, there was a higher rate of recurrence. In both cases described by us, the presence of connection of the ganglion to superior tibiofibular joint along the articular branch was identified intraoperatively.


Spinner et al 15 reported six patients in their series of twenty-four patients who had acute onset of symptoms. Of these, three patients suffered direct blows to the fibular neck region (one of which resulted in a fibular neck fracture), two had been injured during athletic activities and one during a fall. None of those having sudden onset symptoms however occurred spontaneously.


The clinical presentation of these can be striking and therein lies the pitfall of failing to make a timely diagnosis. Swelling may or may not develop at the lateral aspect of knee, and a sensory disturbance over the dorsum of the foot may not occur. Initially only slight weakness in ankle or toe dorsiflexion may exist, but sudden loss of dorsiflexion may occur as well. In most reported series, sudden loss of dorsiflexion is a very rare occurrence. Although ganglion cysts involving the peroneal nerve typically originate from the proximal tibiofibular joint and cause nerve dysfunction secondary to compression, they may alternatively represent cystic degeneration of the nerve sheath and invade nerve, appearing more as intraneural ganglions.5 Regardless of origin, these mucous filled cysts have the potential to grow alongside or even invade nerve, and, in that light, delay in diagnosis can result in irreversible nerve injury.6


The differential diagnosis involves L5 nerve root pathology, 9 post traumatic intraneural haemorrhage, 10,16  a nerve compression near the tendinous arch located at the fibular insertion of the peroneal longus muscle,11  and a nerve sheath tumour.


Clinical examination may not show any obvious swelling. Plain radiographs are of little value in the diagnosis of ganglia, but may be useful in excluding a bony abnormality or fracture of the neck of fibula. Magnetic resonance imaging is most helpful. Seegar and Bassett 12 described the characteristics of ganglia on MRI. On T1-weighted images, the signal intensity is low, whereas on T2-weighted images, the signal intensity is high and they appear homogenous. It may be difficult to differentiate a ganglion from nerve sheath tumours on MRI, as homogeneity of the lesion is also found in solid masses. The evidence of connection between the ganglion cyst and the superior tibiofibular joint capsule or the “tail sign”, can be best seen in axial slices at the level of the joint or on sagittal images.15   Ultrasonography may be useful in showing the cystic nature of the mass and distinguishing it from solid tumours. A combination of MRI and ultrasonography 7 may be helpful in the differential diagnosis of doubtful cases.


It is now well known that a permanent cure can be achieved by microsurgical removal of cyst, respecting the adherent nerve fibres 13 associated with the ligation or electrocoagulation of both the pedicle stalk and recurrent articular branch of the peroneal nerve.14


Obviously when evaluating sudden foot drop, lumbar disc herniation is the first diagnosis considered and if physical examination of spine does not point to one anatomic region as the source of drop, MRI of spine and of the knee may be necessary.  Surgical treatment involves excision of the cyst and exploration of the peroneal nerve 6,7.  There have been reports of the importance of performing preoperative electromyography before embarking on exploration. The justification being that if preoperative electromyography shows tibialis muscle denervation, complete resolution of palsy is less likely 8.

Conclusion

Treatment of ganglion cyst arising from the proximal tibiofibular joint must address the underlying pathoanatomy and should include decompression of the cyst and ligation of the articular branch of the nerve to avoid extraneural recurrence. Resection of the superior tibiofibular joint may also be necessary, but the indications for this additional procedure are not yet well defined.15  Our cases illustrates the consideration of proximal tibiofibular cyst as a cause of sudden foot drop and stress the importance of avoiding delay in making the diagnosis and performing surgical exploration and decompression as soon as the diagnosis is confirmed.

Reference :

  1. Sanders WE. The occult dorsal carpal ganglion. J Hand Surg Br. 1985;10:357-360.

  2. Lowenstein J, Towers J, Matthew MT. Am J Orthop. 2001;30(11):816-819.

  3. Brooks DM. Nerve compression by simple ganglia: a review of thirteen cases. J Bone Joint Surg Br. 1952;34:391-400.

  4. Rawal A, Ratnam KR, Yin Q, Sinopidis C, Frostick S. Compression neuropathy of common peroneal nerve caused by an extraneural ganglion: a report of two cases. Microsurgery. 2004;24(1):63-66.

  5. Spillane RM, Whitmaan CJ, Chew FS. Peroneal nerve ganglion cyst. Am J Roentgenol. 1996;166:682.

  6. Stack RE, Bianco AJ, MacCarty CS. Compression neuropathy of the common peroneal nerve by ganglion cysts. J Bone Joint Surg Am. 1965;47:773-778.

  7. Evans JD, Neumann L, Frostick SP. Compression neuropathy of the common peroneal nerve caused by a ganglion. Microsurgery. 1994;15:193-195.

  8. Parkes A. Intraneural ganglion of the lateral peroneal nerve. J Bone Joint Surg Br. 1961;43:784-790.

  9. Hauax JP, Malghem J, Maldague B, Noel H, Rombouts JJ, Courtois C, Nagant de Deuxchaisnes C. Pathology of the upper peroneotibial joint. History of cysts. Apropos of 4 cases. Rev Rhum Mal Osteoartic. 1986;53:723-726.

  10. Gurdjian ES, Larsen RD, Lindner DW. Intraneural cyst of the peroneal and ulnar nerves. Report of two cases. J Neurosurg. 1965;23;76-78.

  11. Sidey JD. Weak ankles. A study of common peroneal entrapment neuropathy. Br Med J. 1969;3:623-626. 

  12. Seegar LL, Bassett LW. Tumor and tumour like conditions. In: Bassett LW, Gold RH, Seegar LL, editors. MRI: atlas of musculoskeletal system. London: Martin Dunitz; 1989, p319.

  13. Rondepierre P, Martini L, Wannin G, Floquet J. Intraneural cyst: a rare cause of peroneal palsy. Rev Neurol (Paris).1990;146:375-376.

  14. Fransen P, Thauvoy C, Sindic CJM, Stroobandt G. Intraneural ganglionic cyst of the common peroneal nerve: case report and review of literature. Acta Neurol Belg. 1991;91:231-235.

  15. Spinner RJ, Atkinson JLD, Scheithauer BW, Rock MC. Peroneal intraneural ganglia: the importance of articular branch. Clinical series. J Neurusurg. 2003;99:319-329.

  16. Khairallah EW, Weinberg MJ, Maoney J. Acute common peroneal nerve palsy caused by haemorrhage into a recurrent ganglion. Can J Plas Surg. 1995;3:209-211.

 

 

This is a peer reviewed paper 

Please cite as : Rajinder Singh : Sudden Onset Foot Drop From Peroneal Ganglia

J.Orthopaedics 2006;3(4)e20

URL: http://www.jortho.org/2006/3/4/e20

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