Sensory Abnormality E.g. Pain Numbness Paresthesias

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Sensory abnormality (e.g., ache, numbness, paresthesias)? Muscle cramping or aching? Bowel and/or bladder signs? Ocular involvement (e.g., double vision, droopy eyelids)? Bulbar involvement (e.g., voice change)? What activities/movements do you may have hassle with? Duration or sample? Acute-onset suggests a vascular etiology. Fatigability and waxing/waning recommend myasthenia gravis. Weakness distribution: - Proximal vs. Upper vs. decrease extremities? Brainstem infection or inflammation (e.g., sarcoidosis, neuromyelitis optica spectrum disorder). Structural lesion compressing the brainstem. Acute disseminated encephalomyelitis (ADEM). Distribution: Motor and sensory findings could localize to a spinal degree. Reflexes: Upper motor neuron indicators may seem, particularly subacutely (e.g., hyperreflexia, spasticity, Babinski signal). Acutely, patients might have transient spinal shock, with lack of spinal function under the extent of the lesion and areflexia. Sensation: BloodVitals device - Frequently concerned. Sensory stage may be current. Bowel and bladder dysfunction might happen. Spinal cord compression (e.g., trauma, epidural abscess, malignancy). Inflammation (e.g., idiopathic transverse myelitis 📖, neuromyelitis optica spectrum disorders).



Spinal cord infarction (e.g., iatrogenic or complicating meningitis with an area vasculitic course of). Distribution is variable: - Often asymmetric. Enteroviruses (e.g., poliomyelitis, enterovirus D68, enterovirus D71). Arboviruses (e.g., West Nile virus). Paraneoplastic motor neuron disease. Cranial nerve/bulbar involvement: Bulbar involvement may occur, however ocular involvement is rare. Reflexes: Reduced (hyporeflexia or BloodVitals device areflexia). Other findings: Lower motor neuron findings might occur (atrophy, fasciculations). CMV, HIV, EBV, VZV. Vitamin deficiency (e.g., thiamine deficiency; B12 deficiency or BloodVitals monitor nitrous oxide poisoning). Vasculitic neuropathy (e.g., rheumatoid arthritis, polyarteritis nodosa). Toxins: - Heavy metals (e.g., arsenic, mercury). Distribution: - May see proximal limb and neck weakness (similar to myopathy), or descending weakness. Tick paralysis (toxin interferes with acetylcholine launch). Organophosphate poisoning, overdose of anticholinesterases. Distribution: - Proximal limbs and neck are particularly involved. Atrophy might happen (but without fasciculations, as may be seen in decrease motor neuron illness). Metabolic: Hypokalemia (e.g., periodic paralysis). Creatine kinase elevation might suggest myopathy. Consider screening for HIV, if this can be a risk.



TSH (thyroid-stimulating hormone) could also be thought of. CSF is mostly regular in: - Myopathy. Peripheral neuropathies (although CSF abnormalities could happen in neuropathies which contain the nerve roots similar to Guillain-Barre syndrome, CMV, HIV). Guillain-Barre syndrome classically causes albuminocytologic dissociation (elevated protein, despite a normal cell depend). However, elevation of protein might take some time to develop. Forced very important capability is the most important quantity breath the affected person is able to take. Forced vital capacity is an built-in reflection of multiple parameters: inspiratory strength, expiratory power, and lung compliance. The holistic nature of the compelled vital capability might make it a greater predictor of respiratory failure than the unfavourable inspiratory drive (which measures solely diaphragmatic strength). Forced very important capability is more reproducible and fewer uncomfortable than the damaging inspiratory force (mentioned under). This makes the forced vital capability more useful as a serial measurement to trace a affected person's progress over time. Repeated measurements might fatigue patients.



This take a look at has little function in tracking the progress of a affected person with a recognized neuromuscular disorder (e.g., a affected person who has been diagnosed with myasthenia gravis). For the purpose of tracking a patient's trajectory, NIF has not been shown so as to add any independent data past what's provided by the compelled vital capability. The benefit of NIF is that it could more accurately measure muscle energy in a affected person with different pulmonary abnormalities (e.g., in a patient with obstructive lung disease or prior pneumonectomy). Serial pulmonary function assessments are sometimes overutilized. There is no potential evidence that measuring pulmonary perform assessments is helpful. Available data is retrospective and often biased by self-fulfilling prophecy (e.g., patients are intubated based on poor pulmonary mechanics, then subsequently a retrospective research shows that poor mechanics correlate with intubation). Serial pulmonary function testing may interfere with sleep or rest. Serial pulmonary perform testing might cause panic as a consequence of random variation in testing (with sufficient repeat testing, finally the numbers will lower solely as a consequence of random chance).