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Head and Neck
Published in Bobby Krishnachetty, Abdul Syed, Harriet Scott, Applied Anatomy for the FRCA, 2020
Bobby Krishnachetty, Abdul Syed, Harriet Scott
Somatosensory evoked potentials More sensitive compared to EEGCannot detect emboli
Brain death and ethical issues: Death by neurological criteria
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Essentials of Geriatric Neuroanesthesia, 2019
Brittany Bolduc, David M. Greer
Somatosensory evoked potentials (SSEP) is an assessment of the function of the posterior columns, medial lemniscus, thalamus, and sensorimotor cortex. Brain death is indicated by absence of the N20-P22 response to median nerve stimulation bilaterally. The 2010 AAN guidelines reviewed the literature regarding SSEP in brain death determination. Two studies examined the use of nasopharyngeal electrode recording of SSEPs and showed disappearance of the P14 wave (presumably representing medial lemniscus and cuneate nucleus) in all clinically brain-dead patients. The P14 was not absent in the control group of comatose patients who were not brain dead (28,29). There was not adequate statistical precision or investigation to approve this as a recommended ancillary test by the AAN guidelines (4). It is also important to note that SSEP can be normal early in the course of brain death due to some residual functioning neurons, and is presumed to disappear over time (30). Lesions of the upper cervical cord and medulla can also confound results (31).
Brain stimulation: new directions
Published in Alan Weiss, The Electroconvulsive Therapy Workbook, 2018
Somatosensory evoked potentials are a series of waves that reflect sequential activation of neural structures along the somatosensory pathways usually elicited by electrical stimulation of peripheral nerves (Leggatt, 2014). Common sites for electrical stimulation are the posterior tibial nerve at the ankle, the median nerve at the wrist or the peroneal nerve at the knee, with recording electrodes placed on the scalp, over the spine, and over peripheral nerves proximal to the stimulation site. The actual SEP is the result of summated effects of action potentials and synaptic potentials in a volume conductor. The signal generated is subjected to a high level of electrical noise and must be averaged to make the results useful by improving the signal to noise ratio (Evans, 2014).
Chameleons, red herrings, and false localizing signs in neurocritical care
Published in British Journal of Neurosurgery, 2022
Boyi Li, Tolga Sursal, Christian Bowers, Chad Cole, Chirag Gandhi, Meic Schmidt, Stephan Mayer, Fawaz Al-Mufti
Central neurogenic hyperventilation, a syndrome in which hyperpnea and associated respiratory alkalosis occur during both wakefulness and sleep, is considered a result of a pontine lesion, most commonly secondary to tumors.80,85 The exact pathophysiology beyond stimulation of respiratory control areas in the pons and medulla remains unclear.85 When this syndrome is suspected based on clinical presentation, other causes of hyperventilation, such as pulmonary embolus or respiratory disease, must first be ruled out.80 Lesions to the caudal respiratory neurons can cause an apneustic breathing pattern in which each inspiration is accompanied by a prolonged pause.80 As a FLS, this syndrome can also be caused by lower lesions. There have been five reported cases of such apneustic breathing in patients with achondroplasia, the pathophysiology being cervicomedullary compression rather than vagal or pneumotaxic center lesions.86 The lesion’s severity, location, and reversibility by decompression is variable.86 Central neurogenic hyperventilation can also result from thalamic lesions.85 Diagnosis involves polysomnography sleep studies, measuring somatosensory evoked potentials, and CT and MRI scans of the brain.85,86
Neuro-Ophthalmic Literature Review
Published in Neuro-Ophthalmology, 2020
David A. Bellows, Noel C.Y. Chan, John J. Chen, Hui-Chen Cheng, Peter W. MacIntosh, Jenny A. Nij Bijvank, Michael S. Vaphiades
Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune disease that causes severe demyelination, acute optic neuritis and transverse myelitis. The authors report a case of NMOSD and review the disorder. Their case is a 22-year-old man with quadriplegia, urinary incontinence, dyspnoea and visual loss. Spinal magnetic resonance imaging (MRI) showed longitudinal extensive transversal myelitis. The brain MRI was normal, however, brain magnetic resonance spectroscopy showed demyelination. The serum antibody AQP4 (AQP4-IgG) results were seronegative, the cerebrospinal fluid examination was normal, and the oligoclonal band were negative. The ophthalmoscopic examination found bilateral optic atrophy. Somatosensory evoked potential and visual evoked potential examinations were abnormal. The patient was diagnosed with NMOSD and prescribed immunosuppressant therapy, corticosteroids, and therapeutic plasma exchange with significant clinical improvement. This paper reviews NMOSD, the typical clinical presentation, diagnosis, treatment and prognosis.
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
DCM has a broad differential diagnosis that requires a clinician with neurological expertise to decipher. This includes radiculopathy, polyradiculopathy, stroke, inflammation (e.g. multiple sclerosis, transverse myelitis), tumor, Chiari malformation, diabetic neuropathy, peripheral nerve entrapment (e.g. carpal tunnel), and amyotrophic lateral sclerosis (ALS). The diagnosis can typically be made based on the clinical and imaging criteria discussed above, but the possibility of a brain lesion should always be considered and ruled out by a complete neurological examination combined with brain imaging, when necessary. As a result, input from a neurologist, physiatrist, or spine surgeon is necessary to help confirm the diagnosis. In some cases, it is useful for the neurologist or physiatrist to perform electromyography (EMG), nerve conduction studies, and other electrophysiology tests (e.g. somatosensory evoked potentials) to rule out alternative diagnoses. Unfortunately, these tests have poor sensitivity to diagnose cervical myelopathy, but a promising new technique called contact heat evoked potentials (CHEPs) may overcome these limitations [44].