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 Table of Contents  
CASE REPORT
Year : 2017  |  Volume : 7  |  Issue : 1  |  Page : 36-39

Orthostatic intolerance without postural tachycardia complicating lumbar spondylolisthesis


1 Department of Medicine, Ahmadu Bello University, Zaria, Kaduna State, Nigeria
2 Department of Human Physiology, Ahmadu Bello University, Zaria, Kaduna State, Nigeria

Date of Web Publication4-Apr-2018

Correspondence Address:
Dr. S A Abubakar
Department of Medicine, Division of Neurology, Ahmadu Bello University, Zaria, Kaduna State
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ais.ais_47_17

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  Abstract 


Good measure of ability to maintain consciousness during changes in posture is what is termed orthostatic tolerance. Patients with orthostatic intolerance developed symptoms ranging from fatigue, palpitation, dizziness, to syncope on assuming erect from supine position within a short period. Orthostatic intolerance commonly complicates upper spinal cord injury (above T6). Here, we present a case of orthostatic intolerance without significant tachycardia in patient with lumbar spondylolisthesis.

Keywords: Lumbar spondylolisthesis, orthostatic intolerance, tachycardia


How to cite this article:
Abubakar S A, Chukuma P I, Imam M I. Orthostatic intolerance without postural tachycardia complicating lumbar spondylolisthesis. Arch Int Surg 2017;7:36-9

How to cite this URL:
Abubakar S A, Chukuma P I, Imam M I. Orthostatic intolerance without postural tachycardia complicating lumbar spondylolisthesis. Arch Int Surg [serial online] 2017 [cited 2021 May 15];7:36-9. Available from: https://www.archintsurg.org/text.asp?2017/7/1/36/229181




  Introduction Top


Spondylolisthesis is defined as anterior migration or slip of a vertebral body in relation to the vertebral located immediately caudad.[1] Degenerative spondylolisthesis is one of the five categories of spondylolisthesis that is characterized by an intact vertebral ring that is presumed to results from degeneration of facet joint and intervertebral disc with ageing.[2] Spondylolisthesis commonly affect the lumbar and cervical vertebrae and are common among middle aged and elderly adults. Of great clinical concern is the degree of forward slippage that could cause spinal stenosis and nerve root compression. Patients could present with series of symptoms ranging from low back pain, numbness, or weakness of both lower extremities.[3] Patients with high spinal cord injuries, specially cervical and high thoracic (at or above T6) cord lesion could in addition have orthostatic hypotension (OH) or postural hypotension.[4] OH is defined as a fall in systolic blood pressure of at least 20 mmHg or in diastolic blood pressure of at least 10 mmHg within 3 minutes of standing or during a Head-Up Tilt (HUT) of at least 60°.[5] This drop in blood pressure may result in symptoms of orthostatic intolerance associated with increased in heart rate. Symptoms of orthostatic intolerance does not commonly occur in lower thoracic cord lesion or lumbar vertebral body disease. We present here a case of severe orthostatic intolerance without significant tachycardia in a middle-aged man with lumbar spondylolisthesis. This is important because clinicians should note that inability to walk could result from limb weakness or orthostatic intolerance or both in patients with spinal cord lesion.


  Case Report Top


A 47-year-old man presented with four months history of lower back pain, numbness, parasthesia, and progressive weakness of both lower limbs. The symptoms started insidiously, initially with perception of pins and needles sensation in the legs and later lower back pain and limb weakness. The lower limb weakness progressed rapidly within four weeks to complete inability to walk. There was no sphinteric incontinence or features of obstructive uropathy, no history of chronic cough, significant weight loss, or drenching night sweat. There is no antecedent history of febrile illness or gastroenteritis or trauma to the lower back. His past medical history is significant for systemic hypertension controlled on bendrofluazide. There is no premorbid history of episodic dizziness or fainting attacks, his social history is unremarkable. Examination revealed an anxious man with normal neurocognitive assessment (MMSE-29/30) he had flaccid paraparesis, power was 2/5 (MRC) in both lower limbs with normal plantar response. Sensation to light touch and vibration were diminished up to the level of knee joint. His admission pulse rate and blood pressure (at rest and supine position) were 78 beats per minute and 130/70 mmHg, respectively. Examination of chest and abdomen were unremarkable. An empirical diagnosis of lumbar spondylotic radiculopathy to exclude tuberculosis of the spine was made. Available results of requested investigated revealed normal serum urea and electrolyte panel and complete blood count. Erythrocyte sedimentation rate (ESR) was 10 mmfall/hr, Human immunodeficiency virus screening was negative. Electrocardiograph (ECG) revealed normal sinus rhythm, heart rate of 96 beats per minute, features of left ventricular hypertrophy (LVH) using voltage criteria and no features of heart block, while echocardiography showed concentric ventricular hypertrophy with diastolic dysfunction. MRI of lumbar spine revealed destruction of body of L4 and L5 with significant theca compression and narrowing of foramina [Figure 1]. He was managed conservatively with carbamazepine, corticosteroid, and lumbar jacket in addition to deep venous thrombosis (DVT) prophylaxis. He made satisfactory and sustained clinical improvement. The muscle power appreciated to 4/5 in both lower limbs within four weeks of admission. At the time of physical rehabilitation, he developed severe fatigue, dizziness, tremulousness, and pre syncope occasionally associated with nausea and vomiting. These symptoms were provoked by changes in body position when moving from supine to standing and relived by lying flat (supine). These symptoms became very severe that he could not sustain erect position for up to five minutes despite almost normal strength in both lower limbs. Blood pressure taken during this period of orthostatic intolerance revealed a postural drop from 130/70 mmHg supine to 100/60 mmHg standing. The blood pressure at some point dropped to 90/60 mmHg after less than 3 minutes of standing from a normal value of 120/70 mmHg. The radial pulse rate fluctuated between 78 beats per minute to 90 beats per minute. An assessment of orthostatic intolerance without tachycardia was made. Autonomic function test done using non-invasive cardiovascular reflex tests revealed valsalva ratio of 0.96 and 30:15 ratio of 0.86. He was placed on fludrocortisone 2 mg daily. He improved with reduction in orthostatic drop in blood pressure and enhancement of orthostatic tolerance. He could walk without dizzy spells within two weeks of commencement of fludrocortisone.
Figure 1: MRI of lumbosacral spine shows significant compression at L3/L4 and L4/L5 with narrowing of foramina

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  Discussion Top


Orthostatic intolerance is characterised by development of symptoms of cerebral hypoperfusion or sympathetic activation while standing that is relieved by recumbency. They could have diminished concentration and recurrent syncope and these individuals could be incorrectly labelled as having panic attack or anxiety disorder.[6]

Simple activities such as eating showering or low-intensity exercise may profoundly exacerbate these symptoms and could adversely affect quality of life. Patients with autonomic neuropathies such as DM, amyloidosis are at a risk of OH. Not all patients with orthostatic intolerance have autonomic failure or OH.[7] Orthostatic tachycardia is common among patients with orthostatic intolerance making early recognition of the disorder relatively easy. Orthostatic intolerance symptoms commonly occur in the setting of orthostatic hypotension where there is postural drop in blood pressure. This patient developed orthostatic intolerance symptoms with features or evident orthostatic hypotension but no significant tachycardia following lumbar spondylolithesis (T12/L1,2). [Figure 2] review of his cervical MRI revealed no gross lesion. This is not consistent with finding by streeten et al.[7] where orthostatic intolerance (OI) are associated with significant tachycardia. OH occurs commonly in patients with spinal cord injury but occur in patients with cervical and upper thoracic regions [8] as opposed to finding in this index patient.
Figure 2: MRI of cervical spine shows no significant theca compression

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Patients with spinal cord injury could experience symptoms of slight light-headedness, dizziness, blurred vision, fatigue, palpitation, and syncope when they move from lying to sitting or standing position.[9] Loss of cerebral autoregulation and perhaps the rate of fall of individual's blood pressure and not merely the magnitude of the drop in absolute blood pressure may be the factor responsible for the symptoms.[10]

On assuming upright position, several dynamic circulatory responses or changes occur, this include pooling of blood in the leg and extravasation of up to 10% of the plasma into the extravascular space within 10–15 min of passive standing.[11] This pooling of blood and extravasation of plasma could elicit complex neurohumoral reflexes to ensure optimal blood supply to vital organs especially the brain, however, if this persists OH could occur with fainting, but interestingly sympathetically mediated vasoconstriction combined with muscle pumping activity in the leg could counter-balance this effect. In patients with spinal cord injury particularly above T6 (high SCI), there is disruption of efferent from brain stem to sympathetic nerve responsible for vasoconstriction in critical splanchnic circulation and lower limb. This will lead to baroreceptor failure and quick response to blood pressure changes.[12]

Houtman et al.[13] reported that only tetraplegic patients showed poor responses to cardiovascular homeostasis; this is not in keeping with our finding where a paraplegic patient exhibited poor response to cardiovascular homeostasis. The reason for this is not quite clear; however, patients with lumbar sponspondylolithesis have severe reduction muscle tone with gross muscular atrophy. Muscle atrophy may results in inadequate compression of the veins and therefore less effective muscle pump activity. It has also been suggested that venous atrophy may occur coincidentally with muscle atrophy in paralysed limbs resulting in reduced venous compliance.[14] Our patient in addition to severe orthostatic intolerance has poor heart rate response to cerebral hypoperfusion. We cannot clearly explain why, but some patients with orthostatic intolerance after prolonged hospitalization could develop deconditioning and critical illness neuropathy. This may lead to inappropriate response to relative hypovolemia.

In conclusion, orthostatic intolerance could complicate many clinical conditions including lumbar spondylolithesis and because of its heterogeneity in its presentation, clinicians need high index of suspicion to make prompt and accurate diagnosis.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Wiltse LL, Newman PH, Macnab I. Classification of spondylolisis and spondylolisthesis. Clin Orthop Relat Res 1976;117:23-9.  Back to cited text no. 1
    
2.
Rosenberg NJ. Degenerative spondylolisthesis. Predisposing factors. J Bone Joint Surg Am 1975;57:467-74.  Back to cited text no. 2
[PUBMED]    
3.
Vibert BT, Sliva CD, Herkowitz HN. Treatment of instability and spondylolisthesis: Surgical versus nonsurgical treatment. Clin Orthop Relat Res 2006;443:222-7.  Back to cited text no. 3
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4.
Cariga P, Ahmed S, Mathias CJ, Gardner BP. The prevalence and association of neck (coat hanger) pain and orthostatic (postural) hypotension in human spinal cord injury. Spinal Cord 2002;40:77-82.  Back to cited text no. 4
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5.
American Autonomic Society and American Academy of Neurology. Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. Neurology 1996;46:1470.  Back to cited text no. 5
    
6.
Low PA, Opfer-Gehrking TL, Textor SC, Benarroch EE, Shen WK, Schondorf R, et al. Postural tachycardia syndrome (POTS). Neurology 1995;45:S19-25.  Back to cited text no. 6
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7.
Streeten DH, Anderson GH Jr, Richardson R, Thomas FD. Abnormal orthostatic changes in blood pressure and heart rate in subjects with intact sympathetic nervous function: Evidence for excessive venous pooling. J Lab Clin Med 1988;111:326-35.  Back to cited text no. 7
[PUBMED]    
8.
Sidorov EV, Townson AF, Dvorak MF, Kwon BK, Steeves J, Krassioukov A. Orthostatic hypotension in the first month following acute spinal cord injury. Spinal Cord 2008;46:65-9.  Back to cited text no. 8
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9.
Illman A, Stiller K, Williams M. The prevalence of orthostatic hypotension during physiotherapy treatment in patients with an acute spinal cord injury. Spinal Cord 2000;38:741-7.  Back to cited text no. 9
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10.
Hermosillo AG1, Márquez MF, Jáuregui-Renaud K, Cárdenas M. Orthostatic hypotension, 2001. Cardiol Rev 2001;9:339-47.  Back to cited text no. 10
    
11.
van Beekvelt MC1, van Asten WN, Hopman MT. The effect of electrical stimulation on leg muscle pump activity in spinal cord-injured and able-bodied individuals. Eur J Appl Physiol 2000;82:510-6.  Back to cited text no. 11
    
12.
Sampson EE, Burnham RS, Andrews BJ. Functional electrical stimulation effect on orthostatic hypotension after spinal cord injury. Arch Phys Med Rehabil 2000;81:139-43.  Back to cited text no. 12
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13.
Houtman S, Colier WN, Oeseburg B, Hopman MT. Systemic circulation and cerebral oxygenation during head up tilt in spinal cord injured individuals. Spinal Cord 2000;38:158-63.  Back to cited text no. 13
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14.
Mathias CJ, Christensen NJ, Corbett JL, Frankel HL, Goodwin TJ, Peart WS. Plasma catecholamines, plasma renin activity and plasma aldosterone in tetraplegic man, horizontal and tilted. Clin Sci Mol Med 1975;49:291-9.  Back to cited text no. 14
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    Figures

  [Figure 1], [Figure 2]



 

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