Paraplegia as a Complication of Sympathectomy for Hypertension

Mosberg, William H.; Voris, Harold C.; Duffy, James M N

doi:10.1097/00000658-195403000-00010

Cited by 28 publications

(6 citation statements)

References 2 publications

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“…Myelopathy has been described on several occasions following rib resections for sympathectomy (Mosberg et at., 1954;Nathan, 1956;Hughes and MacIntyre, 1963) and following thoracoplasty for tuberculosis (Rouques and Passelecq, 1957) and thoracotomy (Thomas and Dwyer, 1950;Garland et al, 1966, case 2). It is presumed that spinal cord damage is due to operative interruption of blood flow through a major intercostal tributary to the anterior spinal artery, such as that giving rise to the great anterior radicular artery.…”

Section: Myelopathy Following Intercostal Artery Ligationmentioning

confidence: 99%

Non-traumatic ischaemic myelopathy: a review of 25 cases

Kim

Choi

et al. 1988

Spinal Cord

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SummaryThe causes of ischaemic myelopathy are described in 25 patients. Nine developed following surgical manipulation or traumatic laceration of the aorta, 1 following intercostal artery ligation, 3 following aortic aneurysm dissection, 2 following myo cardial infarction and/or cardiac arrest, 7 in the absence of any specifically iden tifiable predisposing factors, and 3 in association with decompression sickness. The degree of clinical recovery was greater among those with incomplete spastic (as opposed to complete flaccid) paralysis and among those in whom sensory loss below the level of injury was incomplete. Despite the diversity of mechanisms that may lead to the development of spinal cord ischaemia, structural damage seems in most instances to affect either grey matter or white matter predominantly. Some of the possible reasons for these preferential sites of damage are discussed. Key words: Ischaemic myelopathy; Paraplegia; Aortic diseases; Spinal vascular disease.There are only a few analytical studies in the English language literature of large series of patients with ischaemic myelopathy, although a number of isolated examples of spinal cord vascular lesions have been published. The most recent reviews of this type include those of Garland, et al. (1966), Mannen (1966, Henson andParsons (1967), andSilver andBuxton (1974). The subject has not been treated in any great detail in standard textbooks of neurology (Adams and Victor, 1985) or neuropathology (Adams, et al., 1984;Davis and Robertson, 1985), probably because of the relatively low frequency with which the condition is encountered. Blackwood (1958), for example, was unable to find a single example of arterial softening of the spinal cord among 3737 postmortem examinations conducted over a 50 year period at the National Hospital, Queen Square.On the arterial side, the better recognised causes of ischaemic myelopathy include recent aortic surgery or traumatic injury, aortic aneurysm dissection,

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Section: Myelopathy Following Intercostal Artery Ligationmentioning

confidence: 99%

Non-traumatic ischaemic myelopathy: a review of 25 cases

Kim

Choi

et al. 1988

Spinal Cord

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“…Subse quently, it was found that this syndrome could also be the result of a fall in perfusion pressure (Garland et al, 1966), or local interference with the spinal cord blood supply (Mosberg et al, 1954;Weisman and Adams, 1944).…”

Section: Introductionmentioning

confidence: 99%

Anterior spinal artery syndrome and its natural history

1983

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Summary. The anterior spinal artery syndrome in three patients is described and from the literature 60 additional patients were collected. Motor recovery in the following groups of patients was noted: (I) Partial loss of motor function and pain sensation-70'4 per cent (19/27); (2) Complete motor loss but partial loss of pain-83 3 per cent (5/6); (3) Paresis but pain sensation absent-66'7 per cent (6/9); and (4) Absent motor function and pain-38-9 per cent (7/18). Motor recovery was also found to vary according to aetiology: (A) Unknown cause-92'9 per cent (13/14); (B) Post-infection or vaccination-88'9 per cent (8/9); (C) Anterior spinal artery occlusion-33'3 per cent (3/9); CD) Spinal cord angioma-20 per cent (2/10); and (E) Aortic lesion-20 per cent (1/5).Patients with sparing of motor function or pain sensation below the lesion do better than those without both functions. Neurological return also varies with the aetiology of the syndrome.

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“…Spillar first described the ASA syndrome secondary to thrombosis [8]. Decreased perfusion pressure [2] and blood vessel compression were also implicated [ 10,11 ]. Necrosis after infarction was suggested to be less extensive than that seen after traumatic spinal cord injury [ 12].…”

Section: Discussionmentioning

confidence: 99%

Cervical Anterior Spinal Cord Infarction

Wilson

Greenberg²,

Barrer

et al. 1992

Journal of Neuroimaging

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Clinical HistoryA 31-year-old, previously healthy man had a sudden onset of sharp interscapular pain, followed by rapidly evolving quadriparesis associated with paresthesias and pain radiating to the anterior part of the chest. Over the next several hours he had difficulty urinating and required catheterization. Three weeks prior to hospitalization, he was treated with erythromycin for an upper respiratory tract infection but had otherwise been well. There was no history of trauma or homosexuality. He did not smoke, drink, or use drugs. On examination, the patient was afebrile with normal vital signs. The general physical examination was only remarkable for moderate obesity. Neurologically, the patient was alert and attentive, with a normal mental status. Cranial nerves were intact and there was no evidence of Homer's syndrome. He exhibited a weak cough but had adequate respiratory function. Motor examination revealed mild weakness of both deltoids and biceps, no function of the triceps or muscles of the forearms and hands, and a flaccid paraplegia. Tendon reflexes were present only in the biceps and were absent in the triceps, patellae, and ankles. Plantar responses were absent. There was no anal wink or superficial abdominal reflexes, and the anal sphincter was flaccid. Sensory examination revealed a level of decreased sensation on the trunk at approximately C-4, below which, including the perianal and inguinal regions, pinprick and temperature sensations were diminished. However, both vibration and joint position sense as well as light touch were preserved in both arms and legs.Laboratory Data: Results of routine chemistries, complete blood cell count, urinalysis, electrocardiography, and chest radiograph were all within normal limits. The sedimentation rate was 17 mm/hr, and antinuclear antibody and rapid plasma reagin test results were negative. Serum protein electrophoresis, cold agglutinins, and Lyme titers were negative or normal. Cerebrospinal fluid analysis revealed 2 white blood cells per cubic millimeter, normal protein and glucose levels, and no oligoclonal bands. Myelography and postmyelographic computed tomography (CT) of the cervical region demonstrated normal findings. Magnetic resonance images (MRis) of the cervical spinal area on admission appeared normal. Cranial MRI and chest CT also showed normal findings. Median nerve somatosensory-evoked potentials revealed 156 Copyright©

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Paraplegia as a Complication of Sympathectomy for Hypertension

Cited by 28 publications

References 2 publications

Non-traumatic ischaemic myelopathy: a review of 25 cases

Non-traumatic ischaemic myelopathy: a review of 25 cases

Anterior spinal artery syndrome and its natural history

Cervical Anterior Spinal Cord Infarction

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