Diagnosis and Evaluation of Acute Paraplegia

1983 ◽  
Vol 4 (10) ◽  
pp. 327-330
Author(s):  
John M. Freeman
Keyword(s):  
Spinal Cord ◽  
Differential Diagnosis ◽  
Adolescent Girl ◽  
Emergency Treatment ◽  
Sudden Onset ◽  
Loss Of Function ◽  
Irreversible Damage ◽  
Spinal Cord Disease ◽  
Acute Paraplegia ◽  
The Brain

CASE REPORT A 14-year-old high school student is admitted to the pediatric neurology service because of the sudden onset of inability to use her legs. When she had gotten up in the morning she was unable to stand. INTRODUCTION Acute neurologic deficit in an adolescent girl (or in anyone else) always represents an emergency requiring immediate evaluation by a physician competent to analyze the deficit, localize its source, develop a differential diagnosis of possible etiologies, organize appropriate tests, and, when indicated, initiate emergency treatment. Acute paraplegia (weakness or paralysis in the legs) is a particular emergency because acute compressive lesions of the cord are reversible. Hours of compression may result in irreversible damage. For this reason neurologic and neurosurgical consultation should be obtained promptly. EVALUATION The evaluation of an individual with an acute paraplegia is best performed with a differential diagnosis in mind. The major cause of paraplegia is spinal cord disease, and its differential diagnosis is shown in Table 1. Spinal cord disease with paraparesis (weakness) may be simulated by lesions in the parasagittal area of the brain, by muscle weakness in the legs (muscular dystrophy or polymyositis), and by conversion reaction. History In evaluating the patient with an "acute" paraplegia one must establish how acute is acute. An immediate total loss of function is almost always vascular.

scholarly journals Snake Eye Appearance; A Rare Radiology Presentation in Acute Flaccid Paralysis: A Case Report

2021 ◽  
Vol 15 (1) ◽  
pp. 43-47
Author(s):  
Mohammad Vafaee-Shahi ◽  
Roghayeh Saeedi ◽  
Neda Pak ◽  
Aina Riahi ◽  
Saeide Ghasemi
Keyword(s):  
Spinal Cord ◽  
Differential Diagnosis ◽  
Brain Stem ◽  
Acute Flaccid Paralysis ◽  
Muscle Tone ◽  
Brain Mri ◽  
Sudden Onset ◽  
Flaccid Paralysis ◽  
Paralytic Poliomyelitis ◽  
The Brain

Background: Acute flaccid paralysis (AFP) is defined by the acute onset of weakness or paralysis with reduced muscle tone in children. There are many non-infectious and infectious causes. Snake eye appearance (SEA) is a rare radiologic appearance and helps narrow down differential diagnoses in flaccid paralysis. Case Presentation: Here, we reported a 6 months-old girl who was admitted with sudden onset flaccid paralysis. She was lethargic and ill without any detectable deep tendon reflexes. She had a high fever that had started 3 days earlier with malaise, poor feeding and coryza. The first child of the family was a boy who expired with similar symptoms; however, the reason is still unknown. Her parents were relatives (cousins). The laboratory and cerebrospinal fluid tests analysis were normal. The brain MRI analysis revealed T1 dim Hypo intensity and T2 hyperintensity along with obvious ADC map hyperintensity in the brain stem. At first, the PCR tests analysis of stool samples for poliovirus and enterovirus were normal. Spinal MRI showed snake eye appearance and helped us narrow our differential diagnosis. We repeated the PCR tests of stool because of snake eye appearance in cervical MRI that was positive for poliovirus and indicated vaccine-associated Paralytic Poliomyelitis (VAPP). Unfortunately, she expired from vaccine associated poliomyelitis. Conclusion: Snake eye appearance is a rare radiologic appearance that can be seen in several pathological conditions; however, it is very rare in patients with acute flaccid paralysis. Radiology signs, especially in spinal cord MRI, can help recognizing abnormalities in images, and narrow the list of differential diagnosis in acute flaccid paralysis. Therefore, spinal cord MRI has an important role in the evaluation of patient with brain stem involvement in acute flaccid paralysis.

scholarly journals Study of clinical profile and outcome of patients with acute non-traumatic paraparesis

2021 ◽  
Vol 10 (1) ◽  
pp. 105
Author(s):  
Sanjana S. Malokar ◽  
Saurabh V. Kothari ◽  
Onkar H. Nadgouda
Keyword(s):  
Spinal Cord ◽  
Peripheral Nerves ◽  
Clinical Presentation ◽  
General Medicine ◽  
Clinical Profile ◽  
Loss Of Function ◽  
Neurological Emergency ◽  
Presenting Symptoms ◽  
Spinal Roots ◽  
Acute Paraplegia

Background: The following study is about the clinical profile and outcome of patients with acute non traumatic paraparesis. It includes the aetiology, clinical presentation and the outcome of various cases of acute non traumatic paraparesis. Paraplegia or paraparesis could be defined as loss of function of both legs as a result of disease or injury of the spinal cord, spinal roots, peripheral nerves or myopathies. Acute non-traumatic paraparesis is a neurological emergency. Reversible causes of acute paraplegia can be treated successfully if diagnosed early.Methods: The observational study was done in the department of general medicine at D. Y. Patil Hospital, Navi Mumbai with sample size of 75 patients over 1 year.Results: With early diagnosis prognosis of acute non traumatic paraparesis can be improved which was evaluated over period of 3 months.Conclusions: Acute non-traumatic paraparesis is a neurological emergency. Reversible causes of acute paraplegia can be treated successfully if diagnosed early. It is important to diagnose and classify all cases into compressive and non-compressive lesions based on presenting symptoms because the management of the two differs.

Transcranial electrical stimulation and intraoperative neurophysiology of the corticospinal tract

2012 ◽  
Author(s):  
Vedran Deletis ◽  
Francesco Sala ◽  
Sedat Ulkatan
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Corticospinal Tract ◽  
Motor Evoked Potentials ◽  
Transcranial Electrical Stimulation ◽  
Irreversible Damage ◽  
Two Factors ◽  
Brain And Spinal Cord ◽  
The Brain ◽  
Wave Collision

Transcranial electrical stimulation is a well-recognized method for corticospinal tract (CT) activation. This article explains the use of TES during surgery and highlights the physiology of the motor-evoked potentials (MEPs). It describes the techniques and methods for brain stimulation and recording of responses. There are two factors that determine the depth of the current penetrating the brain, they are: choice of electrode montage for stimulation over the scalp and the intensity of stimulation. D-wave collision technique is a newly developed technique that allows mapping intraoperatively and finding the anatomical position of the CT within the surgically exposed spinal cord. Different mechanisms may be involved in the pathophysiology of postoperative paresis in brain and spinal cord surgeries so that different MEP monitoring criteria can be used to avoid irreversible damage and accurately predict the prognosis.

The Loss of Function Following on Lesions of the Central Nervous System [Ueber Die Ausfallerscheinungen nach Läsionen Des Central Nervensystems]. (Neurol. Cbl., Nr. 13, 1907.) Rothmann, Max

1908 ◽  
Vol 54 (225) ◽  
pp. 146-148
Author(s):  
William W. Ireland
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Lower Portion ◽  
Loss Of Function ◽  
Cerebral Ganglia ◽  
The Central Nervous System ◽  
Brain And Spinal Cord ◽  
The Brain ◽  
Central Lesions

Rothmann points out how important it is to surgeons that the localisation of lesions in the brain and spinal cord should be made with the utmost accuracy. In many cases diseases do not strike suddenly upon a nervous system previously intact. Often the circulation has been previously deranged by arterial sclerosis, which prepares the way for transitory hemiplegia or aphasia. Sometimes there is loss of function after central lesions, which disappears in longer or shorter time. Goltz and his followers have treated many effects following the extirpation of the whole or part of the cerebrum as due to what they call inhibition (Hemmung). Thus the functions of the spinal cord are much impaired after removal of the cerebral ganglia, or the lower portion of the cord loses its reflex function after section higher up, but after a while it again resumes its act$ibon.

scholarly journals Spinal Arteriovenous Epidural Fistula with Acute Paraplegia

2007 ◽  
Vol 13 (1) ◽  
pp. 75-78 ◽  
Author(s):  
J. Reul ◽  
V. Braun
Keyword(s):  
Spinal Cord ◽  
Emergency Management ◽  
Arteriovenous Fistula ◽  
Emergency Treatment ◽  
Venous Congestion ◽  
Neurological Deficits ◽  
Spinal Angiography ◽  
Acute Paraplegia ◽  
Vascular Myelopathy

We report a case of a 68-year-old woman with an acute paraplegia due to venous congestion of the spinal cord caused by an exclusive epidural arteriovenous fistula. Diagnosed by MRI and selective spinal angiography the fistula was embolized during emergency treatment via transarterial access. Immediately after the intervention the paraplegia declined and the patient recovered completely. Epidural AV fistulae are a very rare and therefore relatively unknown cause of vascular myelopathy. They may require emergency management to avoid permanent neurological deficits.

scholarly journals Acute Paraplegia due to Thoracic Hematomyelia

2016 ◽  
Vol 2016 ◽  
pp. 1-3
Author(s):  
Aykut Akpınar ◽  
Bahattin Celik ◽  
Ihsan Canbek ◽  
Ergun Karavelioğlu
Keyword(s):  
Spinal Cord ◽  
Vascular Malformations ◽  
Case Reports ◽  
Sudden Onset ◽  
Acute Onset ◽  
Good Choice ◽  
High Dose ◽  
Bleeding Disorders ◽  
Solution Methods ◽  
Acute Paraplegia

Spontaneous intraspinal intramedullary hemorrhage is a rare entity with the acute onset of neurologic symptoms. The etiology of idiopathic spontaneous hematomyelia (ISH) is unknown, and there are few published case reports. Hematomyelia is mostly associated with trauma, but the other nontraumatic etiologies are vascular malformations, tumors, bleeding disorders, syphilis, syrinx, and myelitis. MRI is a good choice for early diagnosis. Hematomyelia usually causes acute spinal cord syndrome due to the compression and destruction of the spinal cord. A high-dose steroid treatment and surgical decompression and evacuation of hematoma are the urgent solution methods. We present idiopathic spontaneous hematomyelia of a previously healthy 80-year-old male with a sudden onset of back pain and paraplegia.

Spinal Cord Injury: Preventing Secondary Injury

1992 ◽  
Vol 3 (1) ◽  
pp. 44-54 ◽  
Author(s):  
S. Diane Coen
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Disease Process ◽  
Current Treatment ◽  
Loss Of Function ◽  
Irreversible Damage ◽  
Secondary Damage ◽  
Flexion Extension ◽  
Cord Injury

Spinal cord injury is devastating to the victim, as well as being costly in terms of medical expenses, lost wages, and lost independence. The initial damage to the spinal cord results from several mechanisms of injury—flexion, extension, compression, penetration, rotation, and the disease process. When the spinal cord is injured and there is necrosis of the nervous tissue, no regeneration of that tissue occurs. Unlike in the peripheral nervous system, where regeneration is possible, the spinal cord is part of the central nervous system, as is the brain. The spinal cord extends from the base of the skull to the L1 vertebrae: the cervical levels innervate the diaphragm and muscles of the arms; the thoracic levels innervate the muscles of the chest and abdomen; and the lumbar and sacral levels innervate the muscles of the legs. In addition, the sacral levels are responsible for bowel, bladder, and sexual function. The higher the level of injury, the more severe the loss of function because, not only is the level of injury affected, but also the levels below. Injury occurs by initial trauma to the surrounding ligaments, bones, and muscles, which then affect the spinal cord. There may be total loss of function with damage completely across the cord or partial loss of function with damage affecting only part of the cord. No current treatment can reverse this initial injury, which causes irreversible damage within minutes of injury. Secondary damage occurs as the injury spreads over several hours. Treatment can help prevent this secondary damage

Metallic prions

2004 ◽  
Vol 71 ◽  
pp. 193-202 ◽  
Author(s):  
David R Brown
Keyword(s):  
Prion Protein ◽  
Binding Capacity ◽  
Normal Function ◽  
Transmissible Spongiform Encephalopathies ◽  
Published Data ◽  
Normal Brain ◽  
Copper Binding ◽  
Loss Of Function ◽  
Spongiform Encephalopathies ◽  
The Brain

Prion diseases, also referred to as transmissible spongiform encephalopathies, are characterized by the deposition of an abnormal isoform of the prion protein in the brain. However, this aggregated, fibrillar, amyloid protein, termed PrPSc, is an altered conformer of a normal brain glycoprotein, PrPc. Understanding the nature of the normal cellular isoform of the prion protein is considered essential to understanding the conversion process that generates PrPSc. To this end much work has focused on elucidation of the normal function and activity of PrPc. Substantial evidence supports the notion that PrPc is a copper-binding protein. In conversion to the abnormal isoform, this Cu-binding activity is lost. Instead, there are some suggestions that the protein might bind other metals such as Mn or Zn. PrPc functions currently under investigation include the possibility that the protein is involved in signal transduction, cell adhesion, Cu transport and resistance to oxidative stress. Of these possibilities, only a role in Cu transport and its action as an antioxidant take into consideration PrPc's Cu-binding capacity. There are also more published data supporting these two functions. There is strong evidence that during the course of prion disease, there is a loss of function of the prion protein. This manifests as a change in metal balance in the brain and other organs and substantial oxidative damage throughout the brain. Thus prions and metals have become tightly linked in the quest to understand the nature of transmissible spongiform encephalopathies.

Lessons Learned From Coaching Postsecondary Students With Traumatic Brain Injury

2020 ◽  
Vol 5 (1) ◽  
pp. 88-96
Author(s):  
Mary R. T. Kennedy
Keyword(s):  
College Students ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Sense Of Self ◽  
Scientific Evidence ◽  
Sudden Onset ◽  
Lessons Learned ◽  
Speech Language Pathologists ◽  
The Brain ◽  
Exhaustive List

Purpose The purpose of this clinical focus article is to provide speech-language pathologists with a brief update of the evidence that provides possible explanations for our experiences while coaching college students with traumatic brain injury (TBI). Method The narrative text provides readers with lessons we learned as speech-language pathologists functioning as cognitive coaches to college students with TBI. This is not meant to be an exhaustive list, but rather to consider the recent scientific evidence that will help our understanding of how best to coach these college students. Conclusion Four lessons are described. Lesson 1 focuses on the value of self-reported responses to surveys, questionnaires, and interviews. Lesson 2 addresses the use of immediate/proximal goals as leverage for students to update their sense of self and how their abilities and disabilities may alter their more distal goals. Lesson 3 reminds us that teamwork is necessary to address the complex issues facing these students, which include their developmental stage, the sudden onset of trauma to the brain, and having to navigate going to college with a TBI. Lesson 4 focuses on the need for college students with TBI to learn how to self-advocate with instructors, family, and peers.

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