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title docid authors breadcrumbs category documentVersionId imageCount lastUpdated pageDescription pageKeywords pageTitle enhancedTitle type references breadcrumbs
CIDP 12e4033c-edc8-46ff-8081-3acc433cda78
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b2e6dabb-ee1c-42a4-a332-9f0814c1c607 Surjith Vattoth, MD, FRCR
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Brain brain 6d8829f1-14d7-45af-8675-255189aa526a
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Pathology-Based Diagnoses pathology-based-diagnoses d9d3a8ed-f21b-4831-8c77-591a3500ef77
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CIDP cidp null
Brain 96729e13-6c4b-4fd3-be3e-4e1a940566fd 12 06/08/20 CIDP Brain, Diagnosis, Pathology-Based Diagnoses, Infectious, Inflammatory, and Demyelinating Disease, Inflammatory and Demyelinating Disease, CIDP CIDP | STATdx CIDP DX true
Brain
Diagnosis
Pathology-Based Diagnoses
Infectious, Inflammatory, and Demyelinating Disease
Inflammatory and Demyelinating Disease
CIDP

title: "CIDP" docid: "12e4033c-edc8-46ff-8081-3acc433cda78" authors:

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  • "Brain"
  • "Diagnosis"
  • "Pathology-Based Diagnoses"
  • "Infectious, Inflammatory, and Demyelinating Disease"
  • "Inflammatory and Demyelinating Disease"
  • "CIDP"

KEY FACTS

  • Terminology

    • Clinically heterogeneous, grossly symmetric, sensory & motor neuropathy evolving as monophasic, relapsing, or progressive disorder - Develops over > 8 weeks

  • Imaging

    • Sagittal FLAIR may reveal hyperintense brain lesions similar to multiple sclerosis
    • Enlargement & abnormal T2 hyperintensity of nerve roots, plexi, or peripheral nerves
    • ↑ nerve root diameter, cross-sectional area (CSA), & volume
    • Spinal nerve roots & peripheral nerves (extraforaminal > intradural)
    • Lumbar > cervical, brachial plexus, thoracic/intercostal > cranial nerve
    • Fair degree of CSA correlation between high-resonance nerve ultrasound (HRUS) & MR neurography (MRN)

  • Top Differential Diagnoses

    • Guillain-Barré (AIDP)
    • Inherited demyelinating neuropathy (Charcot-Marie-Tooth)
    • Neurofibromatosis type 1, schwannomatosis

  • Pathology

    • Autoimmune disease of cellular & humoral immunity
    • Hallmarks of CIDP: Enlarged nerves with onion bulb formations, demyelination

  • Clinical Issues

    • Usually clinicaldiagnosis based on progressive weakness/sensory loss & response to steroids
    • Typical: Symmetric proximal & distal weakness, sensory loss
    • Abnormal EMG/NCV: Key electrophysiologic features → nerve conduction block, slowed conduction velocities suggestive of demyelination
    • Diagnosis relies primarily on clinical, electrophysiologic examination supplemented by nerve biopsy

TERMINOLOGY

  • Abbreviations

    • Chronic inflammatory demyelinating polyneuropathy (CIDP)

  • Synonyms

    • Chronic inflammatory demyelinating polyradiculoneuropathy

  • Definitions

    • Chronic acquired, immune-mediated demyelinating neuropathy characterized by relapsing or progressive muscle weakness ± sensory loss

IMAGING

  • General Features

    • Best diagnostic clue

      - Enlargement & abnormal T2 hyperintensity of nerve roots, plexi, or peripheral nerves
- Spinal nerve roots & peripheral nerves (extraforaminal > intradural)
- Lumbar > cervical, brachial plexus, thoracic/intercostal > cranial nerves (CNs)

    • Size

      - Nerve size varies; small → very large
- Mean diameter of spinal nerve roots in CIDP: Cervical 6-6.8 mm; lumbosacral 7.3-10.4 mm
        - 5-mm best cut-off value of C6, C7, C8 nerve root diameters to distinguish CIDP patients from controls
- CIDP nerves larger volumes, which positively correlate with disease duration
- Recent MR neurography (MRN) of L3-S1 nerve roots of lumbosacral plexus using 3D multiple echo recalled gradient-echo (3D MERGE) sequence showed 
        - ↑ mean cross-sectional area (CSA): 28.04 ± 8.55 mm² in CIDP (14.91 ± 2.36 square mm² in normal); optimal cut-off value 19.20 mm²

    • Morphology

      - Focal or diffuse fusiform enlargement of cauda equina, nerve roots/plexi, & peripheral nerves

  • CT Findings

    • NECT

      - Isodense nerve enlargement

    • CECT

      - Mild to moderate nerve enhancement

  • MR Findings

    • T2WI

      - Enlargement, abnormal hyperintensity of intradural & extradural spinal nerves/branches

    • FLAIR

      - Sagittal FLAIR may reveal hyperintense brain lesions similar to multiple sclerosis (MS)

    • DWI

      - Diffusion-weighted MRN
- DTI: ↓ nerve fractional anisotropy (FA) (mean 0.42 ± 0.08) in CIDP compared to healthy controls (0.52 ± 0.04)
        - ↓ FA due to ↑ radial diffusivity (RD); axial diffusivity (AD) not significant
        - FA & RD correlate strongly with electrophysiological markers of demyelination

    • T1WI C+

      - Mild to moderate nerve enhancement

  • Ultrasonographic Findings

    • Grayscale ultrasound

      - Hypoechoic, hypertrophic nerves
- Fair degree of CSA correlation in high resonance nerve US (HRUS) & MRN of cervical plexus, & peripheral nerves in CIDP 
        - CSA in HRUS correlate well with markers of nerve integrity, such as ↓ FA in DTI & with ↑ T2 signal
- HRUS-CSA of interscalene brachial plexus correlated significantly with MRN-CSA & T2 signal of L5 & S1 lumbar plexus roots

  • Imaging Recommendations

    • Best imaging tool

      - MRN, T2WI, enhanced coronal & axial T1WI sequences with fat suppression best delineate nerve lesions
- Brain MR to detect subclinical CNS demyelination

DIFFERENTIAL DIAGNOSIS

  • Conditions Recently Proposed to be Included Under CIDP Syndrome

    • Antimyelin associated glycoprotein (MAG) neuropathy
    • Chronic neuropathies associated with IgG4 antibodies against paranodal/nodal proteins; chronic immune sensory polyradiculopathy (CISP); multifocal motor neuropathy

  • Guillain-Barré (Acute Inflammatory Demyelinating Polyneuropathy)

    • Pial, nerve root enhancement similar to CIDP
    • Differs from CIDP in onset duration, clinical course - Acute onset of ascending paralysis with relative sensory preservation

  • Hereditary Motor and Sensory Neuropathy

    • Also called Charcot-Marie-Tooth (CMT) disease
    • CMT1, CMT 3 (Dejerine-Sottas disease) CMT4, CMTX1
    • Genetic testing, clinical phenotype distinguish from CIDP

  • Neurofibromatosis Type 1

    • Diffuse nerve root enlargement, enhancement
    • Genetic testing & distinctive clinical stigmata to distinguish

  • Lateral Meningocele

    • CSF density/signal intensity (not solid) ± foraminal enlargement, dural ectasia
    • Usually coexisting NF1 or connective tissue disorder (Marfan syndrome)

  • Schwannomatosis

    • Multiple schwannomas of peripheral nerves & CNs [nonvestibular schwannomas (nVS)]
    • However, unilateral VS described with germline mutations of Schwannomatosis in SMARCB1 & LZTR1

  • Other Clinical Differential Diagnosis

    • Diabetic neuropathy, amyloid neuropathy due to TTR mutations, vasculitic neuropathy, POEMS syndrome

PATHOLOGY

  • General Features

    • Etiology

      - Exact pathogenesis of CIDP unclear; involves both cellular & humoral immune factors

    • Polyneuropathies co-occurring with MS: Underdiagnosed; extra disability burden; includes CIDP - 1/3 of MS-CIDP cases with serum testing show IgG4 autoantibodies to neurofascin-155

  • Gross Pathologic & Surgical Features

    • Extensive fusiform nerve enlargement ± gross onion bulb formations

  • Microscopic Features

    • Large nerve, onion bulb formations, demyelination - Macrophage, T-cell infiltration → perivascular inflammatory infiltrates, nerve demyelination & remyelination - Onion bulb formation: Excessive Schwann cell process proliferation → repetitive demyelination/remyelination

CLINICAL ISSUES

  • Presentation

    • Most common signs/symptoms

      - Mixed sensorimotor neuropathy; typical form: Symmetric proximal & distal weakness, sensory loss
- Rarer atypical form (Lewis-Sumner syndrome)
        - Predominantly uni- or multifocal as well as distal
- CNs are occasionally affected, with particular tropism for CNVII, but ophthalmoplegia or bulbar weakness can be present

    • Other signs/symptoms

      - Chronic progressive: Progressively deteriorate until treatment is given

  • Demographics

    • Sex

      - M = F

  • Natural History & Prognosis

    • Average disease duration: 7.5 years

  • Treatment

    • European Federation of Neurological Societies/Peripheral Nerve Society Guideline on management of chronic inflammatory demyelinating polyradiculoneuropathy; immunomodulation or immunosuppression therapy

DIAGNOSTIC CHECKLIST

  • Consider

    • Consider CIDP in differential of nerve root/peripheral nerve enlargement

  • Image Interpretation Pearls

    • MR findings imperfectly correlate with clinical disease activity/severity, laboratory findings

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References

Selected References

  1. Campagnolo M et al: Sporadic hereditary neuropathies misdiagnosed as chronic inflammatory demyelinating polyradiculoneuropathy: Pitfalls and red flags. J Peripher Nerv Syst. 25(1):19-26, 2020
  2. Van den Bergh PYK et al: Boundaries of chronic inflammatory demyelinating polyradiculoneuropathy. J Peripher Nerv Syst. 25(1):4-8, 2020
  3. Wu F et al: MR neurography of lumbosacral nerve roots: diagnostic value in chronic inflammatory demyelinating polyradiculoneuropathy and correlation with electrophysiological parameters. Eur J Radiol. 124:108816, 2020
  4. Suanprasert N et al: Polyneuropathies and chronic inflammatory demyelinating polyradiculoneuropathy in multiple sclerosis. Mult Scler Relat Disord. 30:284-90, 2019
  5. Pitarokoili K et al: High-resolution nerve ultrasound and magnetic resonance neurography as complementary neuroimaging tools for chronic inflammatory demyelinating polyneuropathy. Ther Adv Neurol Disord. 11:1756286418759974, 2018
  6. Ishikawa T et al: MR neurography for the evaluation of CIDP. Muscle Nerve. 55(4):483-9, 2017
  7. Kronlage M et al: Large coverage MR neurography in CIDP: diagnostic accuracy and electrophysiological correlation. J Neurol. 264(7):1434-43, 2017
  8. Kronlage M et al: Diffusion tensor imaging in chronic inflammatory demyelinating polyneuropathy: diagnostic accuracy and correlation with electrophysiology. Invest Radiol. 52(11):701-7, 2017
  9. Said G et al: Chronic inflammatory demyelinative polyneuropathy. Handb Clin Neurol. 115:403-13, 2013
  10. Mahdi-Rogers M et al: Overview of the pathogenesis and treatment of chronic inflammatory demyelinating polyneuropathy with intravenous immunoglobulins. Biologics. 4:45-9, 2010
  11. Tracy JA et al: Investigations and treatment of chronic inflammatory demyelinating polyradiculoneuropathy and other inflammatory demyelinating polyneuropathies. Curr Opin Neurol. 23(3):242-8, 2010
  12. Vallat JM et al: Chronic inflammatory demyelinating polyradiculoneuropathy: diagnostic and therapeutic challenges for a treatable condition. Lancet Neurol. 9(4):402-12, 2010
  13. Van den Bergh PY et al: European Federation of Neurological Societies/Peripheral Nerve Society guideline on management of chronic inflammatory demyelinating polyradiculoneuropathy: report of a joint task force of the European Federation of Neurological Societies and the Peripheral Nerve Society - first revision. Eur J Neurol. 17(3):356-63, 2010
  14. Brannagan TH 3rd: Current treatments of chronic immune-mediated demyelinating polyneuropathies. Muscle Nerve. 39(5):563-78, 2009
  15. Laughlin RS et al: Incidence and prevalence of CIDP and the association of diabetes mellitus. Neurology. 73(1):39-45, 2009
  16. Tazawa K et al: Spinal nerve root hypertrophy on MRI: clinical significance in the diagnosis of chronic inflammatory demyelinating polyradiculoneuropathy. Intern Med. 47(23):2019-24, 2008
  17. Tsuchiya K et al: Demonstration of spinal cord and nerve root abnormalities by diffusion neurography. J Comput Assist Tomogr. 32(2):286-90, 2008
  18. Said G: Chronic inflammatory demyelinating polyneuropathy. Neuromuscul Disord. 16(5):293-303, 2006
  19. Köller H et al: Chronic inflammatory demyelinating polyneuropathy--update on pathogenesis, diagnostic criteria and therapy. Curr Opin Neurol. 18(3):273-8, 2005
  20. Matsuoka N et al: Detection of cervical nerve root hypertrophy by ultrasonography in chronic inflammatory demyelinating polyradiculoneuropathy. J Neurol Sci. 219(1-2):15-21, 2004
  21. Cocito D et al: Different clinical, electrophysiological and immunological features of CIDP associated with paraproteinaemia. Acta Neurol Scand. 108(4):274-80, 2003
  22. Fee DB et al: Resolution of chronic inflammatory demyelinating polyneuropathy-associated central nervous system lesions after treatment with intravenous immunoglobulin. J Peripher Nerv Syst. 8(3):155-8, 2003
  23. Haq RU et al: Chronic inflammatory demyelinating polyradiculoneuropathy in diabetic patients. Muscle Nerve. 27(4):465-70, 2003
  24. Magda P et al: Comparison of electrodiagnostic abnormalities and criteria in a cohort of patients with chronic inflammatory demyelinating polyneuropathy. Arch Neurol. 60(12):1755-9, 2003
  25. Odaka M et al: Patients with chronic inflammatory demyelinating polyneuropathy initially diagnosed as Guillain-Barre syndrome. J Neurol. 250(8):913-6, 2003
  26. Oguz B et al: Diffuse spinal and intercostal nerve involvement in chronic inflammatory demyelinating polyradiculoneuropathy: MRI findings. Eur Radiol. 13 Suppl 4:L230-4, 2003
  27. Press R et al: Aberrated levels of cerebrospinal fluid chemokines in Guillain-Barre syndrome and chronic inflammatory demyelinating polyradiculoneuropathy. J Clin Immunol. 23(4):259-67, 2003
  28. Rodriguez-Casero MV et al: Childhood chronic inflammatory demyelinating polyneuropathy with central nervous system demyelination resembling multiple sclerosis. Neuromuscul Disord. 13(2):158-61, 2003
  29. Ropper AH: Current treatments for CIDP. Neurology. 60(8 Suppl 3):S16-22, 2003
  30. Saperstein DS et al: Current concepts and controversy in chronic inflammatory demyelinating polyneuropathy. Curr Neurol Neurosci Rep. 3(1):57-63, 2003
  31. Toyka KV et al: The pathogenesis of CIDP: rationale for treatment with immunomodulatory agents. Neurology. 60(8 Suppl 3):S2-7, 2003
  32. Costello F et al: Childhood-onset chronic inflammatory demyelinating polyradiculoneuropathy with cranial nerve involvement. J Child Neurol. 17(11):819-23, 2002
  33. Cros D: Peripheral Neuropathy. 1st ed. Philadelphia: Lippincott Williams & Wilkins: 432, 2001
  34. Sabatelli M et al: Pure motor chronic inflammatory demyelinating polyneuropathy. J Neurol. 248(9):772-7, 2001
  35. Saperstein DS et al: Clinical spectrum of chronic acquired demyelinating polyneuropathies. Muscle Nerve. 24(3):311-24, 2001
  36. Taniguchi N et al: Sonographic detection of diffuse peripheral nerve hypertrophy in chronic inflammatory demyelinating polyradiculoneuropathy. J Clin Ultrasound. 28(9):488-91, 2000
  37. Van den Bergh PY et al: Chronic demyelinating hypertrophic brachial plexus neuropathy. Muscle Nerve. 23(2):283-8, 2000
  38. Duarte J et al: Hypertrophy of multiple cranial nerves and spinal roots in chronic inflammatory demyelinating neuropathy. J Neurol Neurosurg Psychiatry. 67(5):685-7, 1999
  39. Midroni G et al: MRI of the cauda equina in CIDP: clinical correlations. J Neurol Sci. 170(1):36-44, 1999
  40. Mizuno K et al: Chronic inflammatory demyelinating polyradiculoneuropathy with diffuse and massive peripheral nerve hypertrophy: distinctive clinical and magnetic resonance imaging features. Muscle Nerve. 21(6):805-8, 1998
  41. Kuwabara S et al: Magnetic resonance imaging at the demyelinative foci in chronic inflammatory demyelinating polyneuropathy. Neurology. 48(4):874-7, 1997
  42. Simmons Z et al: Chronic inflammatory demyelinating polyradiculoneuropathy in children: I. Presentation, electrodiagnostic studies, and initial clinical course, with comparison to adults. 20(12):1569-75, 1997
  43. Van Es HW et al: Magnetic resonance imaging of the brachial plexus in patients with multifocal motor neuropathy. Neurology. 48(5):1218-24, 1997

Images

Selected Images

Sagittal T1 C+ MR of the cervical spine shows marked hypertrophy and enhancement of all exiting cervical nerve roots . 5 mm is considered an adequate cut-off value of cervical spinal nerve root diameter, discriminating CIDP from controls. Mean diameter of spinal nerve roots in CIDP: Cervical 6-6.8 mm; lumbosacral 7.3-10.4 mm. Sagittal T1 C+ MR of the cervical spine shows marked hypertrophy and enhancement of all exiting cervical nerve roots . 5 mm is considered an adequate cut-off value of cervical spinal nerve root diameter, discriminating CIDP from controls. Mean diameter of spinal nerve roots in CIDP: Cervical 6-6.8 mm; lumbosacral 7.3-10.4 mm.

Sagittal T1 C+ MR of the cervical spine shows marked hypertrophy and enhancement of all exiting cervical nerve roots . 5 mm is considered an adequate cut-off value of cervical spinal nerve root diameter, discriminating CIDP from controls. Mean diameter of spinal nerve roots in CIDP: Cervical 6-6.8 mm; lumbosacral 7.3-10.4 mm. Sagittal T1 C+ MR of the cervical spine shows marked hypertrophy and enhancement of all exiting cervical nerve roots . 5 mm is considered an adequate cut-off value of cervical spinal nerve root diameter, discriminating CIDP from controls. Mean diameter of spinal nerve roots in CIDP: Cervical 6-6.8 mm; lumbosacral 7.3-10.4 mm.

Sagittal T1 C+ MR of the cervical spine shows marked hypertrophy and enhancement of all exiting cervical nerve roots . 5 mm is considered an adequate cut-off value of cervical spinal nerve root diameter, discriminating CIDP from controls. Mean diameter of spinal nerve roots in CIDP: Cervical 6-6.8 mm; lumbosacral 7.3-10.4 mm. Sagittal T1 C+ MR of the cervical spine shows marked hypertrophy and enhancement of all exiting cervical nerve roots . 5 mm is considered an adequate cut-off value of cervical spinal nerve root diameter, discriminating CIDP from controls. Mean diameter of spinal nerve roots in CIDP: Cervical 6-6.8 mm; lumbosacral 7.3-10.4 mm.

Sagittal T2WI MR reveals enlargement and T2 hyperintensity of exiting extradural lumbosacral nerves . High signal of CSF should be excluded while measuring nerve root size/area in T2 MR. Sagittal T2WI MR reveals enlargement and T2 hyperintensity of exiting extradural lumbosacral nerves . High signal of CSF should be excluded while measuring nerve root size/area in T2 MR.

Sagittal T2WI MR reveals enlargement and T2 hyperintensity of exiting extradural lumbosacral nerves . High signal of CSF should be excluded while measuring nerve root size/area in T2 MR. Sagittal T2WI MR reveals enlargement and T2 hyperintensity of exiting extradural lumbosacral nerves . High signal of CSF should be excluded while measuring nerve root size/area in T2 MR.

Axial T1WI C+ MR depicts enlargement and abnormal enhancement of exiting extradural lumbosacral nerves . Blood-nerve barrier breakdown can cause contrast enhancement. Axon loss associated with demyelination is the most important factor of disability and resistance to treatment. Root hypertrophy also may cause stenosis symptoms. Axial T1WI C+ MR depicts enlargement and abnormal enhancement of exiting extradural lumbosacral nerves . Blood-nerve barrier breakdown can cause contrast enhancement. Axon loss associated with demyelination is the most important factor of disability and resistance to treatment. Root hypertrophy also may cause stenosis symptoms.

Axial T1WI C+ MR depicts enlargement and abnormal enhancement of exiting extradural lumbosacral nerves . Blood-nerve barrier breakdown can cause contrast enhancement. Axon loss associated with demyelination is the most important factor of disability and resistance to treatment. Root hypertrophy also may cause stenosis symptoms. Axial T1WI C+ MR depicts enlargement and abnormal enhancement of exiting extradural lumbosacral nerves . Blood-nerve barrier breakdown can cause contrast enhancement. Axon loss associated with demyelination is the most important factor of disability and resistance to treatment. Root hypertrophy also may cause stenosis symptoms.

Sagittal FLAIR MR demonstrates periventricular ovoid hyperintensities in a typical case of marked fusiform CIDP nerve enlargement with brain demyelination. Sagittal FLAIR MR demonstrates periventricular ovoid hyperintensities in a typical case of marked fusiform CIDP nerve enlargement with brain demyelination.

Sagittal FLAIR MR demonstrates periventricular ovoid hyperintensities in a typical case of marked fusiform CIDP nerve enlargement with brain demyelination. Sagittal FLAIR MR demonstrates periventricular ovoid hyperintensities in a typical case of marked fusiform CIDP nerve enlargement with brain demyelination.

Additional Images

Axial T1WI C+ MR shows thickening and enhancement of ventral and dorsal cauda equina nerve roots . Axial T1WI C+ MR shows thickening and enhancement of ventral and dorsal cauda equina nerve roots .

Axial T1WI C+ MR shows thickening and enhancement of ventral and dorsal cauda equina nerve roots . Axial T1WI C+ MR shows thickening and enhancement of ventral and dorsal cauda equina nerve roots .

Sagittal T2WI MR demonstrates diffuse thickening of the intradural cauda equina nerve roots. Sagittal T2WI MR demonstrates diffuse thickening of the intradural cauda equina nerve roots.

Sagittal T2WI MR demonstrates diffuse thickening of the intradural cauda equina nerve roots. Sagittal T2WI MR demonstrates diffuse thickening of the intradural cauda equina nerve roots.

Sagittal FLAIR MR of the brain in a CIDP patient shows a typical paraventricular demyelinating lesion similar to those seen in multiple sclerosis patients. Sagittal FLAIR MR of the brain in a CIDP patient shows a typical paraventricular demyelinating lesion similar to those seen in multiple sclerosis patients.

Sagittal FLAIR MR of the brain in a CIDP patient shows a typical paraventricular demyelinating lesion similar to those seen in multiple sclerosis patients. Sagittal FLAIR MR of the brain in a CIDP patient shows a typical paraventricular demyelinating lesion similar to those seen in multiple sclerosis patients.

Sagittal T2WI MR depicts enlarged lumbar nerve roots extending into extraforaminal ventral primary rami . Sagittal T2WI MR depicts enlarged lumbar nerve roots extending into extraforaminal ventral primary rami .

Sagittal T2WI MR depicts enlarged lumbar nerve roots extending into extraforaminal ventral primary rami . Sagittal T2WI MR depicts enlarged lumbar nerve roots extending into extraforaminal ventral primary rami .

Axial T2WI MR shows diffuse thickening and hyperintensity of thoracic nerve roots and paraspinal intercostal nerves. Axial T2WI MR shows diffuse thickening and hyperintensity of thoracic nerve roots and paraspinal intercostal nerves.

Axial T2WI MR reveals bilateral symmetric enlargement, hyperintensity of cervical nerve roots and brachial plexus . Axial T2WI MR reveals bilateral symmetric enlargement, hyperintensity of cervical nerve roots and brachial plexus .

Sagittal T1WI C+ MR demonstrates diffuse pial thickening and enhancement extending into the cauda equina nerve roots. Clinical course distinguished from Guillain-Barré (AIDP). Sagittal T1WI C+ MR demonstrates diffuse pial thickening and enhancement extending into the cauda equina nerve roots. Clinical course distinguished from Guillain-Barré (AIDP).

Axial T2WI MR shows marked enlargement of the lumbar/sacral nerve roots and lumbosacral trunk . Axial T2WI MR shows marked enlargement of the lumbar/sacral nerve roots and lumbosacral trunk .

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