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ISSN: Print -2349-0977, Online - 2349-4387

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Year : 2015  |  Volume : 2  |  Issue : 3  |  Page : 155-157

Visiting beck's syndrome in a teenage boy

1 Department of Neurology, Lakeshore Hospital and Research Centre, Ernakulam, Kerala, India
2 Department of Radiology, Lakeshore Hospital and Research Centre, Ernakulam, Kerala, India
3 Department of Family Medicine, Lakeshore Hospital and Research Centre, Ernakulam, Kerala, India

Date of Web Publication2-May-2016

Correspondence Address:
Muhammed Jasim Abdul Jalal
Department of Family Medicine, Lakeshore Hospital and Research Centre, Nettoor P.O., Maradu, NH 47 Byepass, Ernakulam - 682 040, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2349-0977.181514

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Anterior spinal artery syndrome is caused by occlusion of the anterior spinal artery, which supplies the anterior two thirds of the spinal cord. Here, we report a 14 year old boy, who presented with progressive limb weakness, and urinary retention.

Keywords: Anterior spinal artery occlusion, Beck's syndrome, quadriplegia, snake eye appearance

How to cite this article:
Menon MK, Kandathil JC, Jacob SM, Jalal MJ. Visiting beck's syndrome in a teenage boy. Astrocyte 2015;2:155-7

How to cite this URL:
Menon MK, Kandathil JC, Jacob SM, Jalal MJ. Visiting beck's syndrome in a teenage boy. Astrocyte [serial online] 2015 [cited 2023 Dec 6];2:155-7. Available from: http://www.astrocyte.in/text.asp?2015/2/3/155/181514

  Introduction Top

Anterior spinal artery syndrome (ASAS)––also known as Beck's syndrome––was first described by Spiller (1909) in a patient with anterior spinal artery (ASA) thrombosis, and infarct was noted at autopsy in the anterior part of spinal cord––extending from C4 to T3. It is an extremely rare cause of acute ischemic cord infarction in children. It is caused by occlusion or hypoperfusion of the ASA––which supplies the anterior two-thirds of the spinal cord. The clinical features include loss of motor function below the level of injury, loss of sensations carried by the anterior columns of the spinal cord (pain and temperature), and preservation of fine touch and proprioception (carried by posterior column).

  Case Report Top

A 14-year-old boy presented with acute onset of pain over neck accompanied by numbness of bilateral upper limbs. He had progressive limb weakness, bilateral upper limbs followed within minutes by weakness of both lower limbs, and inability to pass urine. There was no history of any trauma, headache, or fall for except some vigorous neck movements in the form of dance moves of 20 min duration prior to the onset of symptoms. No cranial nerves were involved. On examination, the child was afebrile with a pulse rate of 88/min and blood pressure of 130/80 mmHg. He was conscious and oriented. The pupils were equal and reactive to light with a normal fundus.

The young chap was quadriparetic with power of Grade 1 in right upper limb, Grade 2 in left upper limb, Grade 2 in right lower limb, and Grade 1 in left lower limb. His posterior column sensations were intact although the pain and temperature sensations were lost below C5 level. The child was areflexic with bilateral mute plantar response. There was no evidence of any carotid bruit.

Lumbar puncture was done under aseptic precautions and his cerebrospinal fluid (CSF) study was inconclusive. CSF opening pressure was 120 mm of H2O. Vasculitic work-up was found to be negative for antinuclear antibody, antidouble-stranded DNA, perinuclear antineutrophil cytoplasmic antibody, cytoplasmic antineutrophil cytoplasmic antibody, and antiphospholipid antibody. Thrombophilia screening was also inconclusive as antithrombin, protein C, and protein S were normal. Factor V Leiden mutation was also not detected.

Spiral computed tomography (CT) of cervical spine was normal and did not show any basilar invagination, platybasia, congenital fusion, and block vertebra. CT angiography of the cervical and intracranial arteries was normal. The left vertebral artery was of a smaller caliber as compared to the right side. Basilar artery showed normal caliber. There was no evidence of any thrombus, stenosis, or dissection in any of the vessels. Posterior inferior cerebellar and anterior inferior cerebellar arteries were normally seen. The ASA was not opacified.

Sagittal T2-weighted and axial T2-weighted fat saturation magnetic resonance images (MRIs) through cervical spine demonstrated swollen and edematous cervical cord with T2-weighted high signal anteriorly from C3 to C6-7 levels [Figure 1] and [Figure 2]. Axial postcontrast T1-weighted fat saturation image showed nodular enhancement in either side of the anterior cord with characteristic “snake eye appearance” [Figure 3].
Figure 1: Sagittal T2-weighted and magnetic resonance images through cervical spine demonstrating swollen and edematous cervical cord with T2-weighted high signal anteriorly from C3 to C6-7 levels.

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Figure 2: Axial T2-weighted fat saturation and magnetic resonance images through cervical spine demonstrating swollen and edematous cervical cord with T2-weighted high signal anteriorly from C3 to C6-7 levels.

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Figure 3: Axial postcontrast T1-weighted fat saturation image showed nodular enhancement in either side of anterior cord with characteristic “snake eye appearance.”

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The child was initially pulsed with methyl prednisolone (1 g intravenously once daily for 5 days) and later started on anticoagulation therapy with low molecular weight heparin (enoxaparin sodium – 40 mg subcutaneously twice daily) following imaging.

The child showed mild improvement with physiotherapy and was discharged with steroids in tapering doses and warfarin (8 mg once daily titrated in view of prothrombin time - International Normalized Ratio values) to a rehabilitation center for further physiotherapy and rehabilitation.

The child showed a gradual improvement in his neurological status. After 2 months of intense physiotherapy, he was wheel chair mobilized. His upper limbs showed a remarkable improvement and he was able to feed himself with spoon. After 6 months of physiotherapy and rehabilitation, he was able to stand and walk with support. Even though he is able to sit without support and feed himself, he is still dependent. Physiotherapy and rehabilitation is being continued.

  Discussion Top

The arterial system of the spinal cord is formed by an ASA and two posterior spinal arteries (PSA) with major branches arising from the vertebral, deep cervical, intercostal, and lumbar arteries.[1] The anterior two-third of the spinal cord is supplied by single ASA and it carries motor anterior horn cells, spinothalamic, corticospinal, and autonomic tracts. The posterior one-third is supplied by two PSAs––one on each side––and this portion houses the posterior column. If there is obstruction of ASA, it will lead to motor weakness, loss of pain, temperature and crude touch sensations, and bowel/bladder involvement.

Infarction in the territory of ASA is more frequent than infarction of the posterior ones. Anterior two-thirds of the cord is more frequently affected by ischemia than the posterior one-third due to the existence of more efficient functional anastomoses at the PSA region.[2]

A true anterior spinal cord syndrome results from a vascular lesion at the ASA resulting in ischemic injury to the respective area of the spinal cord. Patients present with complete motor deficits below the lesion, along with sensory deficits affecting pain and temperature sensation. The intensity of the sensory deficits depends on the level of involvement in the spinal cord. Depending on the level of insult, the patient is at risk for autonomic dysreflexia, sexual dysfunction, neuropathic pain, gait impairment, and neurogenic involvement of bowel, bladder, and skin.

The corticospinal and corticobulbar tracts are supplied by the ASA and are affected in ACS. The spinothalamic and spinocerebellar tract can be referred to as the watershed area because of dual vascular supply and location.[3],[4],[5] The sensation is altered depending on the level of involvement at the watershed area. In ACS, sensation to light touch is intact since the blood supply to fasciculus gracilis and cuneatus is from the posterior spinal artery. Interruption of the blood supply to the spinal cord results in irreversible damage to the cord within a short period regardless of the site of interruption.[6] A reduction in blood pressure alone may be enough to cause spinal cord damage. Hypotension added to interruption of the blood supply may augment the damage.

The etiologies of ASA occlusion include:[6]

  • Atherosclerosis
  • Vasculitis
  • Aortic diseases
  • Embolism
  • Cervical spinal trauma
  • Infections and
  • Surgery.

Our patient presented with quadriparesis with dissociated sensory loss. The acute onset of symptoms and subsequent stepwise progression was consistent with ASA occlusion probably due to vigorous neck movements in the form of dance. Cord compression was ruled out by MRI cervical spine. Autoimmune, inflammatory, and infectious etiologies appeared unlikely in view of normal laboratory results. Normal CSF study and the absence of oligoclonal bands in the CSF argued against a demyelinating process. Visual-evoked potential was not done as the anterior horn cell was primarily involved and demyelination was ruled out. Intact posterior column sensations––revealed by a careful and meticulous clinical examination––clinched the diagnosis and the imaging modalities confirmed it.

Successful long-term management of spinal cord injury after the initial hospital stay is dependent upon effective and comprehensive rehabilitation of the patients prior to discharge home. Patients require intensive physical therapy, occupational therapy, and psychological support. Patients and families should be educated about their new diagnosis and associated complications. Patients need to be evaluated for medical equipment to help with mobility and activities of daily living depending on their level of insult. Patients and families need to be trained in caring for and assisting with patient needs. Finally, patients will require long-term psychiatric care for the management of spasticity, neuropathic pain, mobility impairment, and neurogenic skin, bowel, and bladder.

The natural history of ASAS is very acute. Symptoms usually occur very quickly and are often experienced within 1 h of the initial damage. Clinical picture at presentation usually reveals prognosis. Sparing of either motor or sensory function predicts better prognosis as compared to the patients who have both modalities involved. Outcome after 2 months usually depends upon the neurologic deficit at nadir, especially intact proprioception is the predictor of better functional outcome, and early recovery may be because of good collaterals.

  Conclusion Top

ASAS is more of a clinical diagnosis and the crux lies in a complete neurological examination. With typical features of dissociated anesthesia, ASAS is easy to diagnose even though it requires knowledge of existence of such an entity and then a careful physical examination focusing on posterior column is needed. In any case of spinal shock with loss of pain sensation and, where the etiology is not obvious like trauma or fracture, always check the posterior column sensations which if preserved may give you a rare diagnosis of ASAS or Beck's syndrome.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Ramelli GP, Wyttenbach R, von der Weid N, Ozdoba C. Anterior spinal artery syndrome in an adolescent with protein S deficiency. J Child Neurol 2001;16:134-5.  Back to cited text no. 1
Tubbs RS, Blouir MC, Romeo AK, Mortazavi MM, Cohen-Gadol AA. Spinal cord ischemia and atherosclerosis: A review of the literature. Br J Neurosurg 2011;25:666-70.  Back to cited text no. 2
Tureen L. Effects of experimental temporary vascular occlusion on spinal cord, correlation between structural and functional changes. Arch Neurol 1936;35:789.  Back to cited text no. 3
Santos-Franco JA, de Oliveira E, Mercado R, Ortiz-Velazquez RI, Revuelta-Gutierrez R, Gomez-Llata S. Microsurgical considerations of the anterior spinal and the anterior-ventral spinal arteries. Acta Neurochir (Wien) 2006;148:329-38.  Back to cited text no. 4
Sliwa JA, Maclean IC. Ischemic myelopathy: A review of spinal vasculature and related clinical syndromes. Arch Phys Med Rehabil 1992;73:365-72.  Back to cited text no. 5
Kumral E, Polat F, Güllüoglu H, Uzunköprü C, Tuncel R, Alpaydin S. Spinal ischaemic stroke: Clinical and radiological findings and short-term outcome. Eur J Neurol 2011;18:232-9.  Back to cited text no. 6


  [Figure 1], [Figure 2], [Figure 3]


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