Lower back pain and bladder dysfunction
A 36 year old man presented with progressive low back pain and bladder dysfunction. He had had periods of non-specific back
pain for more than a year. In the past two weeks the pain had got worse, radiating from the left dorsolateral thigh to the
lateral site of his left foot. For three days he had had difficulties initiating micturation, and the flow had weakened. He
felt numb sensations in the left scrotum, the perineal region, and on the lateral site of the left foot. He also noticed muscle
weakness in the left foot. He had no history of trauma or recent disease.
General physical examination indicated a healthy young man. Neurological examination showed paralysis of the left foot extensors,
motor weakness of left foot flexors (grade 2-3), and sensory deficits from the medial leg to the dorsal lateral foot. The
patellar reflexes were vivid on both sides (left more than right). The ankle jerk was absent on both sides and plantar flexes
indifferent. Rectal examination indicated saw saddle anaesthesia and low sphincter tone. Normal and crossed straight leg raising
tests were positive at 50° at the left side.
Questions
(1) What worries you most in this case?
(2) What is the term for this complex of symptoms?
(3) What is the differential diagnosis?
(4) What would you do next for this patient?
(5) What are the features seen in the magnetic resonance image (figure1)?
Sagittal T2 weighted magnetic resonance image showing the lumbar spine
(6) What is the diagnosis?
(7) How should you manage this case?
Answers
(1) Alarms should go off when a patient presents with difficulties in micturation and sensory loss in the saddle region. Other
warning signs are the decreased sphincter tone and the motor and sensory loss in the left leg accompanied by acute worsening
of backache.
(2) Cauda equina syndrome is caused by narrowing of the spinal canal: nerve roots become trapped and start to dysfunction.
The array of symptoms can guide the investigator to the level of compression.
(3) All conditions resulting in compression can explain cauda equina syndrome. Consider trauma, disc herniation, spinal stenosis,
neoplasms, spondylolisthesis, inflammatory conditions, and iatrogenic conditions.
(4) Start by taking an accurate history and a clinical examination to narrow the differential diagnosis. You should already
suspect the diagnosis of central disc prolapse. Magnetic resonance imaging is the best diagnostic investigation because it
can depict soft tissues. Consult the orthopaedic or neurological surgeon immediately for further treatment.
(5) The magnetic resonance image in the figure1 shows a massive herniated disc at the level of L4-L5 into the spinal canal. This view also shows some bulging of the disc
at the level of L3-L4 and minor discopathy in the adjacent levels.
(6) Cauda equina syndrome to central disc prolapse at the level of L4-L5.
(7) The suspected diagnosis of central disc prolapse causing cauda equina syndrome is an investigative and surgical emergency.
Surgical decompression should be performed as soon as possible to stop further neurological loss and improve clinical outcome.1 2 3 The preferred method of decompression is laminotomy and partial discectomy.
Discussion
Low back pain is one of the main reasons for a visit to a general practitioner. More than 95% of patients who have low back
pain have a benign musculoskeletal pain syndrome; the pain is a manifestation of a more serious pathology in only 5%.1 4 Central disc prolapse causing cauda equina syndrome is only present in 2% of all cases of a herniated lumbar disc and in
only 0.04% of all patients with low back pain.1 2 4
Herniation of an intervertebral disc is generally the result of degeneration of the disc. The inner nucleus herniates through
the ruptured outside (annulus fibrosus) of the disc. The herniated tissue causes compression of dorsal roots in the spinal
canal, which can result in pain, changed reflexes, and sensory and motor loss.5 The level of the herniation relates to the symptoms (table).5 In most cases lumbar herniations are at the level of L4-L5 or L5-S1.5 6 7 8 Herniation of the intervertebral disc mainly affects men aged 40-50.5 6 7
| Nerve Root |
Pain |
Sensory deficit |
Motor deficit |
Reflex deficit |
| L2 |
Anterior medial thigh |
Upper thigh |
Slight quadriceps weakness; hip flexion; thigh adduction |
Slightly diminished suprapatellar |
| L3 |
Anterior lateral thigh |
Lower thigh |
Quadriceps weakness; knee extension; thigh adduction |
Patellar or suprapatellar |
| L4 |
Posterolateral thigh, anterior tibia |
Medial leg |
Knee and foot extension |
Patellar |
| L5 |
Dorsum of foot |
Dorsum of foot |
Dorsiflexion of foot and toes |
Hamstrings |
| S1-2 |
Lateral foot |
Lateral foot |
Plantar flexion of foot and toes |
Achilles |
| S3-5 |
Perineum |
Saddle |
Sphincters |
Bulbocavernosus; anal |
The rare diagnosis of cauda equina syndrome secondary to central disc prolapse is made on suspicion. Most patients complain
of unilateral or bilateral leg pain and numbness in the perineum or leg or both.2 4 The most sensitive (0.90) and specific (0.95) finding is urinary retention or, later, even incontinence.4 Saddle anaesthesia and decreased sphincter tone on rectal examination, with sensitivities of 0.75 and 0.6-0.8, make the diagnosis
even more plausible.4 Lasègue’s straight leg test, which will cause pain by elongating the nerve root by passive flexion of the hip in a supine
patient, is not very sensitive in this case. Onset can be gradual, as in this man, or sudden with acute trauma related sciatic
pain and problems with vesicular control.2 Unlike most other back problems it may even be painless.
The man had a partial laminotomy, and discectomy at the level of L4-L5 was successfully performed six hours after initial
admission. He was discharged after four days, and apart from minimal sensory loss of his left foot he had no complaints at
three months’ follow up.
Competing interests: None declared.
Provenance and peer review: Not commissioned; externally peer reviewed.
Aernout R J Langeveld orthopaedic resident 1Department of Orthopaedic Surgery, Vrije Universiteit, University Medical Centre, De Boelelaan 1117, 1081 HV Amsterdam, Netherlands
Johannes L Bron orthopaedic resident 1Department of Orthopaedic Surgery, Vrije Universiteit, University Medical Centre, De Boelelaan 1117, 1081 HV Amsterdam, Netherlands
Annemieke J E de Bruijn radiologist 2Department of Radiology, Deventer Ziekenhuis, Fesuvurstraat 7, 7415 CM Deventer, NetherlandsCorrespondence to: A R J Langeveld
Email: aernoutlangeveld@gmail.com
Student BMJ 2008;16:120 | 17
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