Hepatic myelopathy with spastic paraparesis

Utku, Ufuk; Asıl, Talip; Balcı, Kemal; Uzunca, Ilkay; Çelik, Yahya

doi:10.1016/j.clineuro.2004.10.002

Cited by 38 publications

(23 citation statements)

References 7 publications

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“…Motor-evoked potentials, as well as SSEPs and BAEPs, may reveal signs of brainstem dysfunction or myelopathy, even in patients considered to have minimal HE (18)(19)(20)(21)(22)(23), possibly linked to focal oedema occurring in this syndrome, or to concurrent disorders.…”

Section: Evoked Potentialsmentioning

confidence: 99%

Neurophysiological investigations of hepatic encephalopathy: ISHEN practice guidelines

Guérit¹,

Amantini²,

Fischer³

et al. 2009

Liver International

127

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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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Section: Evoked Potentialsmentioning

confidence: 99%

Neurophysiological investigations of hepatic encephalopathy: ISHEN practice guidelines

Guérit¹,

Amantini²,

Fischer³

et al. 2009

Liver International

127

View full text Add to dashboard Cite

show abstract

“…21 In contrast, Nardone et al 5 found an abnormal CMCT to the lower lumbar spinal segments and a normal CMCT to the upper cervical spinal segments, thus supporting localization of main dysfunction to the thoracic spinal cord. Moreover, another MEP study of HM patients indicated that the sites of higher vulnerability are located between the upper thoracic and the lumbar spinal cord.…”

Section: Discussionmentioning

confidence: 95%

Central motor and sensory conduction in patients with hepatic myelopathy

Nardone

Orioli²,

Höller

et al. 2014

Spinal Cord

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Study design: Experimental neurophysiological study. Objectives: The hepatic myelopathy (HM) is characterized by progressive weakness and spasticity of the lower extremities, while there are only a few reports of sensory impairment. However, sensory function has been poorly explored in HM. We believe that an electrophysiological assessment of dorsal columns by somatosensory evoked potentials (SEPs) and of cortico-spinal lateral tracts by motor evoked potentials (MEPs) should be of considerable value in the functional evaluation of the spinal cord involvement in patients with HM. Setting: Salzburg (Austria) and Merano (Italy). Methods: Eight patients diagnosed with HM were studied with MEPs and SEPs. Neurological examination revealed different degrees of cortico-spinal tract involvement in all patients and sensory abnormalities in three patients. Results: Central motor conduction to lower limb muscles was abnormal in all patients, while central sensory conduction was abnormal in seven out of the eight patients. Both central motor and sensory conduction to upper limbs are normal in all patients. Conclusion:The main finding is that electrophysiological evidence of central sensory involvement is present in a very high percentage of patients with HM, and that the threshold for electrophysiological abnormalities is below that for clinical manifestations. Therefore, central sensory and motor conduction studies are sensitive methods for detecting, localizing and monitoring spinal cord damage in HM.

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“…Neuropathological studies demonstrated selective demyelination of the lateral corticospinal tracts with varying degrees of axonal loss. These lesions were seen especially within the cervical levels of the spinal cord but occasionally within the brainstem with no involvement of other tracts [2,3,[6][7].…”

Section: Discussionmentioning

confidence: 99%

“…HEM is usually associated with portal-caval shunts and the patients with HEM survive longer due to medical advances, including liver transplantation [2][3][4] . We report a patient with BuddChiari syndrome and hepatitis B virus (HBV) infection, who developed symptoms and signs of HEM later in life.…”

Section: Introductionmentioning

confidence: 99%

Hepatic encephalomyelopathy: a complication following liver cirrhosis caused by Budd-Chiari syndrome and HBV

Cheng

Jiang

Zhou

et al. 2014

J Infect Dev Ctries

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Progressive encephalomyelopathy is a rare neurological complication of chronic liver disease, even manifesting progressive spastic paraparesis. Few reports detailing the clinical and diagnostic aspects of this uncommon cause of neurological deterioration in patients with hepatic insufficiency have been published. Early recognition of this disorder will become more important in the future as patients with liver disease survive longer due to medical advances, including liver transplantation. The case of a patient with hepatic encephalomyelopathy associated with Budd-Chiari syndrome and HBV-related cirrhosis is presented.

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Hepatic myelopathy with spastic paraparesis

Cited by 38 publications

References 7 publications

Neurophysiological investigations of hepatic encephalopathy: ISHEN practice guidelines

Neurophysiological investigations of hepatic encephalopathy: ISHEN practice guidelines

Central motor and sensory conduction in patients with hepatic myelopathy

Hepatic encephalomyelopathy: a complication following liver cirrhosis caused by Budd-Chiari syndrome and HBV

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