Somatosensory evoked potentials in subclinical portosystemic encephalopathy: A comparison with psychometric tests

Abstract

We prospectively studied the role of somatosensory evoked potentials (SEPs) and psychometric tests in the assessment of subclinical portosystemic encephalopathy (PSE) Evoked potentials are noninvasive, objective electrical manifestations of the nervous system function in response to stimulation. 3,4 Somatosensory evoked potentials (SEPs) can detect the integrity of somatosensory pathways from the peripheral to the central nervous system. 3,4 SEPs are useful in the objective assessment and monitoring of HE in a variety of liver diseases. 5,6 In HE, median nerve-stimulated SEPs showed a progressive prolongation of N20-N65 interpeak latencies (IPLs) correlating with the severity of HE. 6 N20-N65 IPLs have been used in the clinical monitoring of HE, evaluation of the treatment for HE, and prediction of prognosis. [7][8][9][10] In acute and chronic liver disease, approximately one half of the patients with decompensated liver function with grade 0 HE had abnormal prolongation of N20-N65 interpeak latencies. 6,11,12 It is likely that SEP can be of value in the detection of subclinical HE. 13 Therefore, we studied and compared the roles of SEPs and psychometric tests in detection of subclinical HE in cirrhotic patients. PATIENTS AND METHODS Subjects.One hundred consecutive documented cases of cirrhotic patients without clinical HE were studied prospectively at the Cathay General Hospital between 1994 and 1996. Twenty healthy volunteers served as controls. An additional 6 uneducated healthy volunteers underwent only psychometric tests. Sixty-five cirrhotic patients (hepatitis B virus, 30; hepatitis C virus, 28; hepatis B virus and hepatitis C virus, 2; hepatitis B virus and hepatitis D virus, 2; cryptogenic, 3) were included in the present study. Thirty-five cirrhotic patients were excluded because of serious complications and incomplete study. Cirrhosis was diagnosed when patients developed chronic hepatitis with serum alanine transamine (ALT) levels higher than 1.5 times the upper normal limit (normal ALT activity, Ͻ35 IU/L) over a period of more than 6 months, sonographic findings of small liver as well as splenomegaly, and moderate or severe degrees of esophageal varices proven by upper endoscopy.Cirrhotic patients with grade 0 HE were included in the present study. Patients with other neurological diseases and metabolic disorders such as alcoholism, diabetes mellitus, or end-stage renal disease were excluded to avoid coexistent neuropathy or other brain dysfunction. Patients with fever, sepsis, or shock were also excluded to avoid variations caused by body temperature. All cirrhotic patients underwent blood tests, tests for grading of HE and degree of asterixis, psychometric tests, electroencephalography (EEG), and SEPs.Hepatic Encephalopathy. The degree of HE was semiquantified as grade 1 to 4, based on the mental changes proposed by Conn et al. 2 immediately before SEP testing.Blood Tests. Peripheral blood was collected after overnight fasting and within 12 hours of SEP testing for biochemistry at a central lab...

Clinical Neurophysiology of Hepatic Encephalopathy

“…[53][54][55][56][57] Somatosensory evoked potentials (SSEPs) SSEPs explore both nervous transmission from the medulla oblongata to the cortex (central conduction timei.e., the interpeak latency N13-N20-) and hemispheric transmission (middle components of the EP), therefore produce data related to the ones provided by BAEPs and fVEPs, respectively. A minor prolongation of central conduction time in cirrhosis, 37,58 and therefore an alteration in brainstem nervous transmission possibly due to myelopathy or edema was confirmed by SSEPs. However, the prolongation of the middle cortical components (after P25) was found to be much more evident and related with the impairment in neuropsychiatric status 37 and with the risk to develop overt HE in the follow up.…”

“…A minor prolongation of central conduction time in cirrhosis, 37,58 and therefore an alteration in brainstem nervous transmission possibly due to myelopathy or edema was confirmed by SSEPs. However, the prolongation of the middle cortical components (after P25) was found to be much more evident and related with the impairment in neuropsychiatric status 37 and with the risk to develop overt HE in the follow up. 59 These findings prove that HE influences hemispheric multisynaptic pathways more than subcortical brainstem neurotransmission.…”

“…Sensory EPs, as well as motor EPs, produce good estimates of the transmission speed across different areas of the nervous system, providing information on focal edema and myelin fiber dysfunction. [34][35][36][37] Therefore, it is reasonable that they reflect some of the mechanisms that may occur in patients with HE.…”

Nutritional status in non alcoholic subclinical portosystemic encephalopathy

“…The SEP recordings were carried out in a quiet and dimly lit room with the subjects in a supine position using a Dantec Counterpoint ( Dantec Elektronik Medicinsk, Skovlunde, Denmark) by a method as described in previous studies [6,13] . Median nerve evoked cortical responses were recorded for N20-N65 inter-peak latencies ( IPLs ).…”

“…In patients with cirrhosis, malnutrition and increased circulating toxic substances may result in diffuse neuropathy [11,12] . Our subsequent study showed that N20-N65 IPLs of SEPs were helpful in the assessment of subclinical PSE (SPSE), and about a half of cirrhotic patients had SPSE [13] . The role of nutritional status in cirrhotic patients with SPSE remains uncertain.…”