Neurophysiological symptoms

A 36-year-old man developed peripheral polyneuropathy after chronic perianal use of an ammoniated mercury ointment. He had very high blood and urine mercury concentrations. Sural nerve biopsy showed mixed axonal degeneration/demyelination. His symptoms improved progressively over 2 years after withdrawal of the ointment, but neurophysiological recovery was incomplete. 

Peripheral neuropathy with clinical signs and/or symptoms was found in 80% of patients who had received a cumulative dose of 576 mg/m of cisplatin. There was a dose-related reduction in sensory action potential amplitudes (85). The clinical and neurophysiological time progression of the severity of cisplatin polyneuropathy during and after treatment with cisplatin up to a cumulative dose of 600 mg/m has been described (86). 

The investigation of frequent symptoms such as compulsive laughter, yawning and the flow of tears without dysphoria may reveal interesting neurophysiological mechanisms, provided we can isolate and separate the influence of psychological factors in the manifestation of these symptoms. 

Long-term exposure to carbon disulfide via inhalation has been reported to result in neurological effects such as polyneuropathy, neurophysiologic changes, and general depression of nerve conduction velocities in humans. Cardiovascular effects that have been observed following chronic inhalation of carbon disulfide vapors by workers include generalized symptoms of heart disease, vascular... 

Basso (2010)[56] Colorectal (40) FOLFOX 4, FOLFOX 6 CT naive and not CT naive (but neurotoxicity naive) Caucasian CAG motif of SK3 Neurophysiological examination, acute toxicity symptoms scale A short CAG repeats allele (13—15 repeats) associated to higher incidence of severe acute 28 (11, severe)... 

Sharief M, Pridden J, Delamont R et al. (2002). Neurophysiologic evaluation of neuromuscular symptoms in UK Gulf War veterans. A controlled study. Neurology, 59, 1518-1525. 

The majority of patients with clinically overt HE show alterations of the EEG with an increasing amount of theta and delta rhythms with increase in the grade of HE (Davies et al., 1991 Montagnese, Amodio and Morgan, 2004 Parsons-Smith et al., 1957). Like the clinical symptoms, these EEG alterations, however, are unspecific. Thus, the EEG cannot be used to prove the diagnosis of HE. This also holds true for other neurophysiological methods such as evoked potentials. 

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