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OPLL
Published in Kelechi Eseonu, Nicolas Beresford-Cleary, Spine Surgery Vivas for the FRCS (Tr & Orth), 2022
Kelechi Eseonu, Nicolas Beresford-Cleary
This patient demonstrates clinical signs of cervical myelopathy. I would request X-rays of the cervical spine (AP and lateral) to evaluate the sagittal alignment of the cervical spine. I would also request an MRI scan. A CT scan of the cervical spine would allow me to exclude ossification of either the PLL or the OLF. If these were normal, I would also perform an upper limb nerve conduction study to exclude peripheral neuropathy as a cause of the symptoms.
The spine
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
Degenerative change in the cervical spine leading to spinal cord compression is the commonest cause of cervical myelopathy in patients over 55 years of age. Lower motor neurone changes occur at the level of the lesion, with atrophy of the upper extremity muscles, particularly the intrinsic muscles of the hands. Upper motor neurone findings are noted below the level of the lesion and may involve both upper and lower extremities. If surgery is considered appropriate then an anterior or posterior decompression may be required.
The neck
Published in Ashley W. Blom, David Warwick, Michael R. Whitehouse, Apley and Solomon’s System of Orthopaedics and Trauma, 2017
Tests for cervical myelopathy The following are physical findings suggestive of upper motor neuron compromise and cervical myelopathy: Hoffmann’s sign – involuntary flexion of the thumb and index finger distal phalanx by flicking of the terminal phalanx of the middle fingerfinger escape sign – little finger abduction when the patient is asked to stretch his or her hands in frontfinger fatigue test – patient fatigues when asked to open and close his or her fists quicklyLhermitte’s sign – an electric shock-like sensation along the spine if the spine is flexedclonus – rapid movements of the feet triggered by forceful passive motion of the ankle into dorsiflexion from a plantar position.
Multidisciplinary approach to degenerative cervical myelopathy
Published in Expert Review of Neurotherapeutics, 2020
Ali Moghaddamjou, Jamie R.F. Wilson, Allan R. Martin, Harry Gebhard, Michael G. Fehlings
The clinical signs of DCM are varied and often subtle, thus requiring assessment by an expert clinician. Common symptoms include upper extremity numbness, fine motor dysfunction (i.e. clumsiness) of the hands, imbalance when walking, and bladder dysfunction such as urgency or incontinence; these symptoms form the basis for the widely used modified Japanese Orthopedic Association (mJOA) scale, which is arguably the most relevant measure of the severity of cervical myelopathy [38]. However, patients may also present with a variety of other symptoms including weakness, lower extremity numbness, L’Hermitte’s phenomenon (shock-like pain up and down the spine), neck pain, cervicogenic headache, and muscle spasm. Clinical signs of cervical myelopathy include focal motor deficit, muscle wasting, hyperreflexia, Hoffman’s sign, Babinsky sign, dysdiadochokinesia, sensory deficits (particularly to pain/temperature), gait ataxia (including tandem gait), and Romberg sign. Unfortunately, not all health care practitioners are adequately educated about the signs and symptoms of DCM as part of their routine training, and efforts are needed to address this gap. Primary care physicians, advanced nurse practitioners, and physiotherapists can be trained to make these clinical assessments with a particular focus in mastering the mJOA.
High field structural MRI in the management of degenerative cervical myelopathy
Published in British Journal of Neurosurgery, 2018
Dan Wright, Sean Martin, Erlick AC Pereira, Yazhuo Kong, Irene Tracey, Thomas Cadoux-Hudson
Cervical radiculopathy can be acute and if so is often caused by disc herniation. This often occurs in younger patients. The cytokine mediated milieu that ensues predominately effects large diameter myelinated axons causing motor symptoms. Chronic radiculopathy more often presents with sensory disturbances. Compression of the nerve root causes local dural and arachnoid thickening and alteration to the blood-nerve barrier leading to nerve root dysfunction.12 The clinical findings often point to the affected cervical level. Cervical myelopathy is a form of chronic spinal cord injury. The resultant compression of neural structures causes hypoperfusion injury. The anterior and posterior spinal arteries are compromised, and in turn the pial and intramedullary arterioles.13 Venous congestion causes venous infarction. Hypoxia damaged oligodendrocytes and neurons cause an inflammatory response which along with ischaemic endothelial cell damage causes compromise of the blood-spinal cord barrier (BSCB). Inflammatory Fas ligand (FasL) signalling then leads to neuronal loss and axonal damage.11
Clinical outcomes following conservative management of chronic traumatic cervical myelopathy: A case report
Published in Physiotherapy Theory and Practice, 2018
Justin Bridges, Roberto Sandoval
Myelopathy can be defined as a clinical syndrome that occurs from a functional disturbance or pathological change of the spinal cord that interferes with normal transmission of neural impulses (Columbia University Department of Neurological Surgery 2014). Cervical myelopathy – myelopathy associated with the cervical spine – results from a mechanism of degeneration, neurological disease, vascular compromise, abnormal growth, osteophyte formation, or trauma (Baptiste and Fehlings 2006; Cook et al. 2011; Salvi et al. 2006; Thelen et al. 2014). Preexisting cervical spine degenerative, postural, or structural changes may predispose a person to cervical myelopathy during a traumatic event (Baptiste and Fehlings 2006; Rhee et al. 2013). Traumatic cervical myelopathy caused by a whiplash mechanism is a result of excessive force(s). Whiplash experienced in a MVA alters subsequent hyperflexion or hyperextension of the cervical spine (Baptiste and Fehlings 2006).