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Examine the lower limbs
Published in Hani TS Benamer, Neurology for MRCP PACES, 2019
Q: What are the causes of monoplegia? Cerebrovascular disease (sudden onset).Brain tumour (gradual onset).Spinal cord lesion (gradual onset).
Posture and orthopedic impairments
Published in Michael Horvat, Ronald V. Croce, Caterina Pesce, Ashley Fallaize, Developmental and Adapted Physical Education, 2019
Michael Horvat, Ronald V. Croce, Caterina Pesce, Ashley Fallaize
A complete spinal cord lesion (injury) results in absence of sensation and motor function below the level of that injury. An incomplete lesion, in which the cord is not completely transected, results in varying amounts of sensation and motor functioning below the injury. Injuries may involve several levels, such as T2–T4 (interfering with functioning from the second thoracic to fourth thoracic vertebra). This type of injury will also be characterized by the availability of more functioning ability on one side of the body (VHI, 2017c, d)
Injuries of the spine
Published in Ashley W. Blom, David Warwick, Michael R. Whitehouse, Apley and Solomon’s System of Orthopaedics and Trauma, 2017
‘Spinal shock’ The physiological dysfunction following structural injury rarely lasts for more than 48 hours. Below the level of the injury, the muscles are flaccid, the reflexes are absent and sensation is lost. While the primitive reflexes (anal ‘wink’ and the bulbocavernosus reflex) are absent, there is spinal shock and the neurological level cannot be accurately determined. The bulbocavernosus reflex is commonly elicited by tugging on the Foley catheter during a digital rectal exam. If an anal contraction occurs, the bulbocavernosus reflex is present and the patient is out of spinal shock. A complete spinal cord lesion cannot be diagnosed in the presence of spinal shock, as the neurological level may still improve.
Feasibility, safety, and functional outcomes using the neurological controlled Hybrid Assistive Limb exoskeleton (HAL®) following acute incomplete and complete spinal cord injury – Results of 50 patients
Published in The Journal of Spinal Cord Medicine, 2023
Mirko Aach, Thomas Armin Schildhauer, Amrei Zieriacks, Oliver Jansen, Martin Weßling, Alexis Brinkemper, Dennis Grasmücke
Fifty patients with acute incomplete and complete SCI (14 females, 36 males) participated in this prospective study. All patients were in the acute phase of SCI. In all patients, the time interval between SCI and the onset of HAL® training was less than one year (mean time 117.98 ± 95.82 days; range 4–327 days). All patients were classified prior to training according to the American Spinal Injury Association Impairment Scale (AIS). SCI lesions were located between C4 and L4 (AIS A-D). Sixteen subjects suffered from tetraplegia, and 34 from paraplegia. Three patients were classified as AIS grade A with no motor sensory function in the sacral segments S4/S5, but with zones of partial preservation (ZPP) below the lesion level. 30 patients were categorized as AIS grade C. Seventeen patients were classified as AIS grade D. No subject was classified as AIS grade B. Thirty-nine of the subjects had suffered traumatic spinal cord injuries. In four patients, massively prolapsed intervertebral discs caused incomplete paraplegia and in one patient, an epidural abscess with spondylodiscitis caused the SCI. In one patient, intramedullary cavernoma, and in another patient, anterior spinal artery syndrome caused the spinal cord lesion. One patient suffered from tuberculosis with osteolysis of the vertebra T7-T10. In one patient, a tumor infiltrated the spinal canal, one patient suffered cervical spinal canal stenosis and cervical myelopathy and in one patient, ischemic myelopathy caused the spinal cord lesion. Mean age ± SD at the time of enrollment was 43.88 ± 15.0 years (range, 18–72 years).
Longitudinally extensive transverse myelitis preceding primary central nervous system lymphoma: Spinal sentinel neuroinflammation
Published in The Journal of Spinal Cord Medicine, 2023
Merve Hazal Ser, Bade Güleç, Ayşe Salihoğlu, Uğur Uygunoğlu
Two months later, her paraparesis fully recovered, while sensorial disturbances and incontinence were recovered partially. Thoracic MRI demonstrated that the lesion involving T4-T9 segments was completely regressed, and cranial, cervical, and lumbar MRI were also normal. Nine months after the LETM, she was admitted to the emergency unit with subacute encephalopathy, and her cranial imaging revealed a left caudothalamic compressive T2 hyperintense lesion with peripheral gadolinium enhancement. At this time, repeated thoracic MRI also confirmed that there was no recurrence of the spinal cord lesion. Cerebral biopsy resulted in diffuse large B-cell lymphoma. Primary central nervous system lymphoma (PCNSL) was diagnosed since bone marrow biopsy and whole-body PET-CT were normal. The initial LETM episode was granted as spinal sentinel neuroinflammation. Rituximab was initiated and cranial lesion regressed, spinal cord lesion did not recur at her recent follow-up visit 2 years after the LETM.
Inpatient rehabilitation outcomes in neoplastic spinal cord compression vs. traumatic spinal cord injury
Published in The Journal of Spinal Cord Medicine, 2022
Sevgi Ikbali Afsar, Sacide Nur Saraçgil Cosar, Oya Umit Yemişçi, Hüma Bölük
The medical records of a total of 338 patients consisting of 209 (61.8%) traumatic SCI patients and 129 (38.2%) non-traumatic SCI patients were reviewed. Neoplastic causes were found in 43 (33.3%) of the non-traumatic SCI patients. Low-grade malignant tumors (schwannoma, astrocytoma, ependymoma and meningioma) of the spine or spinal cord were present in 22 (51.2%) patients in the neoplastic group. A metastatic spinal cord lesion was found in 16 (37.2%) patients and other rare causes included multiple myeloma (3 patients), plasmacytoma (1 patient) and lymphoma (1 patient) (Table 1). Metastatic spinal cord compression was due to lung cancer in 5 (11.6%) patients, prostate in 5 (11.6%) patients, breast cancer 2 (4.7%) patients, colon cancer in 2 (4.7%) patients, and renal cell carcinoma in 2 (4.7%) patients. The cause of traumatic SCI was primarily motor vehicle accident (45.4%) followed by fall from height (42.1%) (Table 1).