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Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Spinal cord compression differential diagnosis

Introduction

Overview

Overview

Acute spinal cord compression presents with sudden onset of paralysis along with back pain, it must be differentiated from other diseases with similar presentation such as muscle weakness and back pain. Transverse myelitis, GBS (Gullian-Barrie syndrome), HIV-myopathy, diabetic neuropathy, multiple sclerosis (MS), amyotrophic lateral sclerosis(ALS) and peripheral neuropathies are some of the diseases to be considered in the differential.[1][2][3][4][5][6][7][8][9]

Differentiating Spinal Cord Compression from other Diseases

Differentiating Spinal Cord Compression from other Diseases

Acute spinal cord compression presents with sudden onset of paralysis along with back pain, it must be differentiated from other diseases with similar presentation such as muscle weakness and back pain. Transverse myelitis, GBS(Gullian-Barrie syndrome), HIV-myopathy, diabetic neuropathy, multiple sclerosis (MS), amyotrophic lateral sclerosis(ALS) and peripheral neuropathies are some of the diseases to be considered in the differential. The following table describes the differentiating signs and symptoms of other diseases from an acute spinal cord compression.[1][2][3][4][5][6][7][8][9]

Disease/Condition Differentiating Signs/Symptoms Differentiating Tests
CSF Findings Other diagnostic tests
Transverse myelitis Febrile illness preceding the symptoms

Lower extremity > Upper extremity

Pleocytosis

↑Total protein

Focal demyelination on MRI
Gullian-Barre syndrome (GBS) History of gastroenteritis or influenza-like illness

Ascending paralysis

Loss of deep tendon reflexes

Respiratory muscle weakness requiring ventilation

Albumin-cytologic dissociation

↑Total protein

EMG shows decreased conduction.

Seropositive for Campylobacter jejuni (50% cases).

HIV-related myelopathy History of HIV infection

Paraparesis, spasticity or ataxia coupled with dementia

Nonspecific ELISA positive, followed by confirmation with Western blot.
Amyotrophic lateral sclerosis (ALS) Combination of UMN and LMN lesion symptoms

Muscle weakness and stiffness as the initial symptoms

Nonspecific Fibrillation potentials and positive sharp waves, with fasciculation potentials on EMG
Multiple sclerosis Mimic clinical symptoms of spinal compression.

All cases involve the brain.

Presents with multiple episodes separated by space with self-resolution

Visual symptom (neuromyelitis optica) distinct for MS

↑ IgG and oligobands MRI brain shows areas of demyelination.
Diabetic neuropathy History of diabetes mellitus.

Pain and loss of sensation in the feet in a glove-and-stocking distribution.

Bladder dysfunction may be present due to autonomic neuropathy.

Nonspecific EMG shows reduction in sensory nerve conduction and a decrease in amplitude.
Polymyositis Symmetrical weakness of shoulder and pelvic girdles. Nonspecific EMG include spontaneous fibrillations, low-amplitude short-duration polyphasic motor potentials.

Muscle biopsy shows immune cell infiltration and destruction of muscle fibers.

Hereditary muscular dystrophy Proximal and distal muscle weakness

Without sensory changes in the initial stages.

Nonspecific MRI and EMG/nerve conduction studies will show only myopathic changes
References

References

  1. ↑ 1.0 1.1 Beh, Shin C.; Greenberg, Benjamin M.; Frohman, Teresa; Frohman, Elliot M. (2013). “Transverse Myelitis”. Neurologic Clinics. 31 (1): 79–138. doi:10.1016/j.ncl.2012.09.008. ISSN 0733-8619.
  2. ↑ 2.0 2.1 van Doorn PA (2013). “Diagnosis, treatment and prognosis of Guillain-Barré syndrome (GBS)”. Presse Med. 42 (6 Pt 2): e193–201. doi:10.1016/j.lpm.2013.02.328. PMID 23628447.
  3. ↑ 3.0 3.1 Di Rocco A, Simpson DM (1998). “AIDS-associated vacuolar myelopathy”. AIDS Patient Care STDS. 12 (6): 457–61. doi:10.1089/apc.1998.12.457. PMID 11361993.
  4. ↑ 4.0 4.1 Kiernan MC, Vucic S, Cheah BC, Turner MR, Eisen A, Hardiman O, Burrell JR, Zoing MC (2011). “Amyotrophic lateral sclerosis”. Lancet. 377 (9769): 942–55. doi:10.1016/S0140-6736(10)61156-7. PMID 21296405.
  5. ↑ 5.0 5.1 Rowland LP, Shneider NA (2001). “Amyotrophic lateral sclerosis”. N. Engl. J. Med. 344 (22): 1688–700. doi:10.1056/NEJM200105313442207. PMID 11386269.
  6. ↑ 6.0 6.1 Loma I, Heyman R (2011). “Multiple sclerosis: pathogenesis and treatment”. Curr Neuropharmacol. 9 (3): 409–16. doi:10.2174/157015911796557911. PMC 3151595. PMID 22379455.
  7. ↑ 7.0 7.1 Goldenberg MM (2012). “Multiple sclerosis review”. P T. 37 (3): 175–84. PMC 3351877. PMID 22605909.
  8. ↑ 8.0 8.1 Bansal V, Kalita J, Misra UK (2006). “Diabetic neuropathy”. Postgrad Med J. 82 (964): 95–100. doi:10.1136/pgmj.2005.036137. PMC 2596705. PMID 16461471.
  9. ↑ 9.0 9.1 Hunter K, Lyon MG (2012). “Evaluation and management of polymyositis”. Indian J Dermatol. 57 (5): 371–4. doi:10.4103/0019-5154.100479. PMC 3482800. PMID 23112357.