Metronidazole Induced Encephalopathy in a Patient with Brain Abscess

Metronidazole is commonly used for brain abscess but is not well known for its neurotoxic complications. Metronidazole-induced encephalopathy (MIEP) is toxic encephalopathy associated with the use of metronidazole. We experienced a case of brain abscess which developed reversible severe MIEP during treatment period. Although MIEP occurs in typical locations, it is not easy to differentiate from other conditions such as cerebral infarction, demyelinating diseases and metabolic diseases. Neurosurgeons should be aware that severe MIEP can occur during the use of metronidazole though it is not common.     

Metabolic Encephalopathy: Behind the Name

Metabolic encephalopathy may be the most common diagnosis in consultative acute neurology. The origin of this term is not generally known but can be traced back. The term replaced more commonly used designations such as organic or functional. The term metabolic encephalopathy was originally linked to organ dysfunction but subsequently became more imprecise. When it expanded to include a large number of diseases, it evolved to “metabolic neuronal dysfunction” and soon could not be distinguished from “quiet delirium” and other designations. This vignette summarizes why the terminology has confused more than clarified but also why it will likely stay in the neurologist’s vernacular.     

Rett syndrome: clinical presentation and laboratory investigations in 12 further French patients

Twelve French patients with the Rett syndrome collected since July 1982 are reported. They confirm the stereotyped clinical presentation of the syndrome which represented 22% of the whole progressive encephalopathies referred to our hospital in the same period and 55% of the progressive encephalopathies of unknown etiology. Metabolic investigations have been constantly negative.     

Metabolic encephalopathies

Kinnier Wilson coined the term metabolic encephalopathy to describe a clinical state of global cerebral dysfunction induced by systemic stress that can vary in clinical presentation from mild executive dysfunction to deep coma with decerebrate posturing; the causes are numerous. Some mechanisms by which cerebral dysfunction occurs in metabolic encephalopathies include focal or global cerebral edema, alterations in transmitter function, the accumulation of uncleared toxic metabolites, postcapillary venule vasogenic edema, and energy failure. This article focuses on common causes of metabolic encephalopathy, and reviews common causes, clinical presentations and, where relevant, management.     

Triphasic waves: clinical correlates and morphology

Twenty-six (41%) of 63 consecutive patients with triphasic waves had various types of metabolic encephalopathies while 37 patients (59%) had non-metabolic encephalopathies, usually senile dementia. Triphasic waves were not found to be specific for any single type of metabolic encephalopathy. Etiology was more closely linked to conscious level at recording than any morphological or distributional feature of the triphasic waves themselves. Thus, all 31 alert patients had non-metabolic encephalopathies while all 13 comatose patients had metabolic encephalopathies. The second, positive, component (Wave II) most often had the highest voltage while equally maximal Waves I and II occurred next most commonly. Triphasic waves were most often maximally expressed anteriorly. Among patients with metabolic encephalopathies, a posterior-anterior delay or lag of the wave II peak occurred more commonly than did the better known anterior-posterior lag. Lags occurred with both metabolic and non-metabolic conditions, but were more common with the former. No difference in quantity or mode of appearance existed between the metabolic and non-metabolic groups when matched for conscious level. Prognosis for patients with either metabolic or non-metabolic encephalopathies was unfavourable. Only 4 of 24 metabolic and one of 35 non-metabolic patients were well at follow-up over 2 years later. Forty percent of EEGs with sharp and slow wave complexes (slow spike waves) had sporadically-appearing triphasic waves. The relative amplitudes of the 3 components differed from triphasic waves in other conditions: equally maximal Waves II and III were the most usual form.     

Steroid-responsive encephalopathy in autoimmune thyroiditis: Clinical spectrum and MRI observations in three cases

Hashimoto''s encephalopathy (H.E.) is probably of autoimmune etiology, and manifests with seizures, stroke-like episodes, cognitive decline, neuropsychiatric symptoms, myoclonus. It is presumed to be autoimmune in origin with high serum titers of antithyroid peroxidase antibodies (anti-TPA). Thyroid function might often be normal. The diagnosis is arrived at by excluding other toxic, metabolic and infectious causes of encephalopathies, supportive clinical profile, elevated thyroid antibodies and optimum steroid response. We present the characteristic phenotypic manifestations, magnetic resonance imaging and electroechography observations and response to immunomodulation with follow-up in three cases of H.E. All the three cases manifested with subacute to chronic progressive encephalopathy, cerebellar dysfunction, seizures, behavioral abnormalities and oculomotor disturbances and had evidence of hypothyroidism, elevated titers of anti-TPA and positive thyroid anti-microsomal antibodies. Atypical and uncommon presentations are known. This report emphasizes that a high index of suspicion is often required in cases with “investigation negative encephalopathy” for early diagnosis of H.E.     

The nosologic panorama of progressive ataxia in Swedish children

Described are 76 children with a picture of progressive encephalopathy and ataxia as the principal or joint principal leading signs. The series was hospital-based in Gothenburg between 1973 and 1983, and not representative for epidemiologic analyses. The children were divided in groups by using a combined pathogenetic and clinical grouping system: lysosomal disorders (6 children), non-lysosomal lipid disorders (10), intermediary metabolic disorders (3), heredoataxias (22), phacomatoses including Louis-Bar (5), dysimmune encephalopathies (6), other defined disorders (19) and undefined or incompletely defined conditions (5). Different groups are discussed and, according to this material, a diagnostic pathway is drawn up.     

Neurologic manifestations of hepatic disease

Neurologic complications of hepatic disease are not uncommon and involve the CNS more often than the peripheral nervous system or muscles. Progress in the therapy of neurologic disorders associated with hepatic failure has occurred in recent years. Notably, exciting developments in the treatment of hepatic encephalopathy with benzodiazepine antagonists will lead to a better understanding of the pathophysiology of this encephalopathy. The future use of these agents may eventually help reduce the morbidity and mortality of hepatic encephalopathy. The role of this class of drug in other metabolic encephalopathies remains to be established. Furthermore, new therapeutic and surgical alternatives to the treatment of Wilson disease also enhance our therapeutic options. The fate of patients with Wilson disease with fulminant hepatic disease and those patients unable to tolerate or unresponsive to penicillamine therapy has been greatly improved.     

Acute necrotizing encephalopathy with widespread edematous lesions of symmetrical distribution

Summary A 67-year-old Japanese woman with liver cirrhosis was affected by an unusual acute progressive encephalopathy, presenting mental confusion and slurred speech as its initial symptoms. She died in profound coma, following the entire course of 17 days. Autopsy disclosed bilateral symmetrical, widespread, edematous and necrotic lesions, their centers being located in the basal ganglia, diencephalon and midbrain, and their peripheries expanding into the cerebral white matter, cerebellum, pons and medulla. Diapedesis of erythrocytes and serum plasma was conspicuous, in contrast to paucity of capillary proliferation. Although the lesions were somewhat similar to those of Wernicke's and Leigh's encephalopathies, they were considered to be representative of a more acute metabolic disorder distinct from the latter conditions.     

The many faces of human prion diseases in Belgium and the world

Prion diseases are rare neurodegenerative disorders that always lead to death and that can be transmissible under certain conditions. Although sporadic Creutzfeldt-Jakob's disease (CJD) is the best known human variant of these transmissible spongiform encephalopathies with an incidence of about 1 in 106 inhabitants, several other types of human prion disease have been described (e.g. Familial CJD, Gerstmann-Str?ussler-Scheinker syndrome, Fatal Familial Insomnia,...). In 1996, a variant of CJD has been linked to the epidemic of bovine spongiform encephalopathy (BSE). Therefore, vigilance concerning prion diseases was increased throughout the whole of Europe. In Belgium, a comprehensive, nation-wide study has been conducted both retrospectively (1960-1997) and prospectively (1998-...) to identify prion disease patients. In 1998, a surveillance system has also been created to monitor the incidence of CJD and other prion diseases. Using data from both studies and the surveillance program, the occurrence and phenotype of all types of prion diseases in Belgium was investigated. The sporadic type of CJD was identified in 116 patients, while 4 suffered from a hereditary form. In our series, we could find no evidence for variant or iatrogenic CJD, neither for the more rare types of prion diseases.