By studying neuronal activity through neuronal electrogenesis, neurophysiological investigations provide a functional assessment of the nervous system and, therefore, has been used for quantitative assessment and follow-up of hepatic encephalopathy (HE). The different clinical neurophysiological approaches can be classified depending on the function to explore and their sensitivity to HE. The reliable techniques are those that reflect cortical function, i.e., cognitive-evoked potentials (EPs) (P300 paradigm), electroencephalogram (EEG), visual EPs (latency 4 100 ms) and somatosensory EPs (SEPs) (latency between 25 and 100 ms). Short-latency EPs (brainstem acoustic EPs, SEPs of a latency o 25 ms) are in principle insensitive to HE, but can disclose brainstem conduction deficits due to oedema. SEPs and motor EPs can disclose myelopathies. Because of its parallelism to the clinical examination, clinical neurophysiology can complement the neurological examination: (i) to provide evidence of HE in patients who have normal consciousness; (ii) to rule out, at least under some conditions, disturbances of consciousness due to other causes (e.g. drug-induced disturbances, nonconvulsive status epilepticus) with the reservation that the mildest degrees of encephalopathy might be associated with an EEG pattern similar to that induced by drugs; and (iii) to demonstrate the worsening or, conversely improvement, of HE in the follow-up period.By studying neuronal activity through central or peripheral neuronal electrogenesis, neurophysiological investigations provide a functional assessment of the nervous system. Therefore, their domain is similar to that of the clinical examination and complementary to that of neuroimaging. When compared with the clinical examination, they provide a more quantitative assessment, potentially amenable for follow-up, and may remain interpretable in patients under muscle blockade, in whom clinical examination is not feasible.Because neuronal electrogenesis depends on neuronal activity that is sensitive to the influence of energyproviding metabolic systems as well as to the influence of those systems that are involved in electrolyte homoeostasis and clearance of toxic substances, clinical neurophysiology has been used for quantitative assessment and follow-up of metabolic encephalopathies (1). Neurophysiological techniquesTwo techniques are available for routine use, both in clinical and in experimental settings: the electroencephalogram (EEG) and evoked potentials (EPs). Recommendations for their execution are reported by Deuschl and Eisen (2). The grading of recommendations in this article was performed according to the EASL criteria (Table 1).The EEG primarily reflects cortical neuronal activity modulated by both physiological and pathological diencephalic and brainstem influences and by metabolic and toxic factors. Many abnormal EEG patterns are

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Laser pulses selectively excite mechano‐thermal nociceptors and evoke brain potentials that may reveal small‐fiber dysfunction. We applied CO2‐laser pulses to the perioral and supraorbital regions and recorded the scalp laser‐evoked potentials (LEPs) and reflex responses in the orbicularis oculi, masticatory, and neck muscles in 30 controls and 10 patients with facial sensory disturbances. Low‐intensity pulses readily evoked scalp potentials consisting of a negative component with a latency of 165 ms followed by a positive component at 250 ms. In vertex recordings, the amplitude of LEPs exceeded 30 μV. Although only high‐intensity pulses evoked reflex responses, some subjects showed—even to low‐intensity pulses—an orbicularis oculi (blink‐like) response that markedly contaminated the scalp recording. Scalp LEPs were abnormal in patients with hypalgesia and normal trigeminal reflexes and normal in patients with normal pain sensitivity and abnormal trigeminal reflexes. Possibly because of the high receptor density in this area and the short conduction distance, laser stimulation of the trigeminal territory yields low‐threshold and large LEPs, which are useful for detecting dysfunction in peripheral and central pain pathways. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 508–516, 1999.

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Objectives: To evaluate the accuracy of the peroneal nerve test (PENT) in the diagnosis of critical illness polyneuropathy (CIP) and myopathy (CIM) in the intensive care unit (ICU). We hypothesised that abnormal reduction of peroneal compound muscle action potential (CMAP) amplitude predicts CIP/CIM diagnosed using a complete nerve conduction study and electromyography (NCS-EMG) as a reference diagnostic standard. Design: prospective observational study. Setting: Nine Italian ICUs. Patients: One-hundred and twenty-one adult (≥18 years) neurologic (106) and non-neurologic (15) critically ill patients with an ICU stay of at least 3 days. Interventions: None. Measurements and main results: Patients underwent PENT and NCS-EMG testing on the same day conducted by two independent clinicians who were blind to the results of the other test. Cases were considered as true negative if both NCS-EMG and PENT measurements were normal. Cases were considered as true positive if the PENT result was abnormal and NCS-EMG showed symmetric abnormal findings, independently from the specific diagnosis by NCS-EMG (CIP, CIM, or combined CIP and CIM). All data were centrally reviewed and diagnoses were evaluated for consistency with predefined electrophysiological diagnostic criteria for CIP/CIM.During the study period, 342 patients were evaluated, 124 (36.3%) were enrolled and 121 individuals with no protocol violation were studied. Sensitivity and specificity of PENT were 100% (95% CI 96.1-100.0) and 85.2% (95% CI 66.3-95.8). Of 23 patients with normal results, all presented normal values on both tests with no false negative results. Of 97 patients with abnormal results, 93 had abnormal values on both tests (true positive), whereas four with abnormal findings with PENT had only single peroneal nerve neuropathy at complete NCS-EMG (false positive). Conclusions: PENT has 100% sensitivity and high specificity, and can be used as a screening test to diagnose CIP/CIM in the ICU.

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