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Compression Physiology: Nerves and Roots.

The site of injury within the olfactory system differs with various agents (Cometto-Muñiz and Cain 1991). For example, ethyl acrylate and nitroethane selectively damage olfactory tissue while the respiratory tissue within the nose is preserved (Miller et al. 1985). Formaldehyde alters the consistency, and sulphuric acid the pH of nasal mucus. Many gases, cadmium salts, dimethylamine and cigarette smoke alter ciliary function. Diethyl ether causes leakage of some molecules from the junctions between cells (Schiffman and Nagle 1992). Solvents, such as toluene, styrene and xylene change olfactory cilia; they also appear to be transmitted into the brain by the olfactory receptor (Hotz et al. 1992). Hydrogen sulphide is not only irritating to mucosa, but highly neurotoxic, effectively depriving cells of oxygen, and inducing rapid olfactory nerve paralysis (Guidotti 1994). Nickel directly damages cell membranes and also interferes with protective enzymes (Evans et al. 1995). Dissolved copper is thought to directly interfere with different stages of transduction at the olfactory receptor level (Winberg et al. 1992). Mercuric chloride selectively distributes to olfactory tissue, and may interfere with neuronal function through alteration of neurotransmitter levels (Lakshmana, Desiraju and Raju 1993). After injection into the bloodstream, pesticides are taken up by nasal mucosa (Brittebo, Hogman and Brandt 1987), and can cause nasal congestion. The garlic odour noted with organophosphorus pesticides is not due to damaged tissue, but to detection of butylmercaptan, however.

Environmental agents can gain access to the olfactory system through either the bloodstream or inspired air and have been reported to cause smell loss, parosmia and hyperosmia. Responsible agents include metallic compounds, metal dusts, nonmetallic inorganic compounds, organic compounds, wood dusts and substances present in various occupational environments, such as metallurgical and manufacturing processes (Amoore 1986; Schiffman and Nagle 1992 (). Injury can occur both after acute and chronic exposures and can be either reversible or irreversible, depending on the interaction between host susceptibility and the damaging agent. Important substance attributes include bioactivity, concentration, irritant capacity, length of exposure, rate of clearance and potential synergism with other chemicals. Host susceptibility varies with genetic background and age. There are gender differences in olfaction, hormonal modulation of odorant metabolism and differences in specific anosmias. Tobacco use, allergies, asthma, nutritional status, pre-existing disease (e.g., Sjogren's syndrome), physical exertion at time of exposure, nasal airflow patterns and possibly psychosocial factors influence individual differences (Brooks 1994). Resistance of the peripheral tissue to injury and presence of functioning olfactory nerves can alter susceptibility. For example, acute, severe exposure could decimate the olfactory neuroepithelium, effectively preventing spread of the toxin centrally. Conversely, long-term, low-level exposure might allow preservation of functioning peripheral tissue and slow, but steady-transit of damaging substances into the brain. Cadmium, for example, has a half-life of 15 to 30 years in humans, and its effects might not be apparent until years after exposure (Hastings 1990).

Physiology of the Spinal Cord, Nerve Root and Peripheral Nerve Compression.

Nerve Root Compression Model Flashcards | Quizlet

AB - Previous animal experiments suggest that mild compression may increase susceptibility of nerve roots to the effects of hypotention. The authors report the case of patient with an unstable L2 burst fracture whose motor skills and senses were intact. During fracture reduction and spinal distraction, sensory- evoked potentials were recorded from the epidural space after right and left femoral and tibial nerve stimulation. Induced hypotension was used during the surgery. All responses were normal at the outset of the surgery. With hypotension, a marked drop in the amplitude of the right femoral evoked potential amplitude occurred; left femoral and both tibial responses remained unchanged. Evoked potential changes were reversible with reversal of hypotension. Postoperatively, the patient was neurologically intact. Further analysis revealed a significant correlation between the right femoral evoked potential amplitude and systolic blood pressure (r = 0.63, P

(11-16) More recently, Epstein indicated that nerve root entrapment and compression may be responsible for such things as sciatica; intermittent claudication, an ischemic condition; and other similar types of conditions.

the nerve root compression hypothesis is far from obsolete

N2 - Previous animal experiments suggest that mild compression may increase susceptibility of nerve roots to the effects of hypotention. The authors report the case of patient with an unstable L2 burst fracture whose motor skills and senses were intact. During fracture reduction and spinal distraction, sensory- evoked potentials were recorded from the epidural space after right and left femoral and tibial nerve stimulation. Induced hypotension was used during the surgery. All responses were normal at the outset of the surgery. With hypotension, a marked drop in the amplitude of the right femoral evoked potential amplitude occurred; left femoral and both tibial responses remained unchanged. Evoked potential changes were reversible with reversal of hypotension. Postoperatively, the patient was neurologically intact. Further analysis revealed a significant correlation between the right femoral evoked potential amplitude and systolic blood pressure (r = 0.63, P

Background: The Scratch Collapse Test (SCT) is used to assist in the clinical evaluation of patients with ulnar nerve compression. The purpose of this study is to introduce the hierarchical SCT as a physical examination tool for identifying multilevel nerve compression in patients with cubital tunnel syndrome.

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Ulnar Nerve Compression | Living Handbooks


Boards: Nerve Compression Flashcards | Quizlet

N2 - Introduction Different hypotheses have been proposed for the pathophysiology of posterior interosseous nerve (PIN) palsy, namely compression, nerve inflammation, and fascicular constriction. We hypothesized that critical reinterpretation of electrodiagnostic (EDX) studies and MRIs of patients with a diagnosis of PIN palsy could provide insight into the pathophysiology and treatment. Materials and methods We retrospectively reviewed patients with a diagnosis of nontraumatic PIN palsy and an upper extremity EDX and MRI. The original EDX studies and MRIs were reinterpreted by a neuromuscular neurologist and musculoskeletal radiologist, respectively, both blinded to our hypothesis. Results Fifteen patients met the inclusion criteria, i.e., having an “isolated” PIN palsy. Four patients (27%) had a defined mass compressing the PIN. The remaining 11 patients (73%) presented with at least one finding incompatible with the compression hypothesis: physical examination revealed that weakness in muscles was not innervated by the PIN in 4 patients (36%); EDX abnormalities not related to the PIN were found in 4 patients (36%); and reinterpretation of the MRIs showed muscle atrophy or nerve enlargement beyond the territory of the PIN in 9 patients (82%), without any evidence of compression of the PIN in the proximal forearm. Conclusion The eleven patients in our series with presumed isolated and idiopathic PIN palsy had evidence of a more diffuse nerve–muscle involvement pattern, without any radiologic signs of nerve compression of the PIN itself. These data would favor an inflammatory pathophysiology when a structural lesion compressing the nerve is ruled out with imaging.

Start studying Boards: Nerve Compression

AB - Introduction Different hypotheses have been proposed for the pathophysiology of posterior interosseous nerve (PIN) palsy, namely compression, nerve inflammation, and fascicular constriction. We hypothesized that critical reinterpretation of electrodiagnostic (EDX) studies and MRIs of patients with a diagnosis of PIN palsy could provide insight into the pathophysiology and treatment. Materials and methods We retrospectively reviewed patients with a diagnosis of nontraumatic PIN palsy and an upper extremity EDX and MRI. The original EDX studies and MRIs were reinterpreted by a neuromuscular neurologist and musculoskeletal radiologist, respectively, both blinded to our hypothesis. Results Fifteen patients met the inclusion criteria, i.e., having an “isolated” PIN palsy. Four patients (27%) had a defined mass compressing the PIN. The remaining 11 patients (73%) presented with at least one finding incompatible with the compression hypothesis: physical examination revealed that weakness in muscles was not innervated by the PIN in 4 patients (36%); EDX abnormalities not related to the PIN were found in 4 patients (36%); and reinterpretation of the MRIs showed muscle atrophy or nerve enlargement beyond the territory of the PIN in 9 patients (82%), without any evidence of compression of the PIN in the proximal forearm. Conclusion The eleven patients in our series with presumed isolated and idiopathic PIN palsy had evidence of a more diffuse nerve–muscle involvement pattern, without any radiologic signs of nerve compression of the PIN itself. These data would favor an inflammatory pathophysiology when a structural lesion compressing the nerve is ruled out with imaging.

Nerve compression physiology | myINSiGHT

Introduction Different hypotheses have been proposed for the pathophysiology of posterior interosseous nerve (PIN) palsy, namely compression, nerve inflammation, and fascicular constriction. We hypothesized that critical reinterpretation of electrodiagnostic (EDX) studies and MRIs of patients with a diagnosis of PIN palsy could provide insight into the pathophysiology and treatment. Materials and methods We retrospectively reviewed patients with a diagnosis of nontraumatic PIN palsy and an upper extremity EDX and MRI. The original EDX studies and MRIs were reinterpreted by a neuromuscular neurologist and musculoskeletal radiologist, respectively, both blinded to our hypothesis. Results Fifteen patients met the inclusion criteria, i.e., having an “isolated” PIN palsy. Four patients (27%) had a defined mass compressing the PIN. The remaining 11 patients (73%) presented with at least one finding incompatible with the compression hypothesis: physical examination revealed that weakness in muscles was not innervated by the PIN in 4 patients (36%); EDX abnormalities not related to the PIN were found in 4 patients (36%); and reinterpretation of the MRIs showed muscle atrophy or nerve enlargement beyond the territory of the PIN in 9 patients (82%), without any evidence of compression of the PIN in the proximal forearm. Conclusion The eleven patients in our series with presumed isolated and idiopathic PIN palsy had evidence of a more diffuse nerve–muscle involvement pattern, without any radiologic signs of nerve compression of the PIN itself. These data would favor an inflammatory pathophysiology when a structural lesion compressing the nerve is ruled out with imaging.

Nerve compression physiology; ..

Methods: A prospective cohort study (2010–2011) was conducted of patients referred with primary cubital tunnel syndrome. Five ulnar nerve compression sites were evaluated with the SCT. Each site generating a positive SCT was sequentially “frozen out” with a topical anesthetic to allow determination of both primary and secondary ulnar nerve entrapment points. The order or “hierarchy” of compression sites was recorded.

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