Atypical Metronidazole-Induced Encephalopathy in Anaerobic Brain Abscess

Metronidazole-induced encephalopathy is a very rare complication of the long standing use of metronidazole. The encephalopathy is bilateral and symmetric in nature. We report on the magnetic resonance imaging (MRI) and clinical course of metronidazole-induced encephalopathy in a 60-year-old female with a persistent anaerobic brain abscess after draining of the abscess. After 3 months of metronidazole administration, the patient complained of dysarthria, tingling sense of all extremities, and left hemiparesis. MRI revealed symmetric hyperintensity lesions in medulla, pons, dentate nuclei of cerebellum, and splenium of corpus callosum, all of which represent typical findings of metronidazole-induced encephalopathy. In addition, asymmetric lesions in midbrain, thalamus, putamen and cerebral subcortical white matter were noted. The patient recovered after discontinuation of metronidazole and the remaining abscess was successfully treated with meropenem and levofloxacine.     

Metronidazole-induced encephalopathy and inferior olivary hypertrophy: lesion analysis with diffusion-weighted imaging and apparent diffusion coefficient maps

BACKGROUND: Although several cases of metronidazole-induced encephalopathy have been reported, to our knowledge, there is no previous report of brain changes in anterior commissure, basal ganglia, cerebellar white matter, and inferior olivary nuclei on magnetic resonance images. The precise mechanisms of action of metronidazole-induced encephalopathy have not been determined. OBJECTIVES: To report a unique case of metronidazole-induced encephalopathy extensively involving multiple lesions and to determine the precise mechanism of action of metronidazole-induced encephalopathy. SETTING: University hospital.Patient A 74-year-old woman hospitalized with complaints of progressive dysarthria, dysphagia, and gait disturbance 3 months after the initiation of metronidazole therapy.Intervention Brain magnetic resonance imaging and discontinuation of metronidazole therapy.Main Outcome Measure We observed changes of multiple lesions found on magnetic resonance imaging and analyzed apparent diffusion coefficient map values. RESULTS: Initial fluid-attenuated inversion recovery brain magnetic resonance images showed high signal intensities in diffuse subcortical white matter, anterior commissure, splenium, basal ganglia, midbrain, cerebellar white matter, and bilateral inferior olivary nuclei. These lesions were resolved after discontinuation of metronidazole therapy. However, the lesions in the inferior olivary nuclei were not resolved; rather they became hypertrophic. Apparent diffusion coefficient map values in the symptom period decreased and were normalized after discontinuation of metronidazole therapy. CONCLUSIONS: We describe a patient with metronidazole-induced encephalopathy involving reversible lesions in the anterior commissure, basal ganglia, and cerebellar white matter, which have not been reported previously. We observed inferior olivary hypertrophy, believed to be the result of lesions in the midbrain and cerebellar white matter rather than the result of lesions induced by metronidazole therapy. By using diffusion-weighted imaging and apparent diffusion coefficient maps, we found that metronidazole-induced encephalopathy might be caused by cytotoxic edema.     

Episodic encephalopathy due to an occult spinal vascular malformation complicated by superficial siderosis

Superficial siderosis (SS) of the central nervous system is a rare condition caused by chronic subarachnoid hemorrhage. Clinical manifestations typically include sensorineural hearing loss and cerebellar ataxia. Recurrent episodic encephalopathy in the setting of SS has not been reported. We describe a unique case of SS in a 67-year-old man with an 8-year history of episodic encephalopathy associated with headache and vomiting. The patient also had a history of progressive dementia, ataxia, and myelopathy. A diagnosis of superficial siderosis was made after magnetic resonance gradient-echo images showed diffuse hemosiderin staining over the cerebellum and cerebral convexities. No intracerebral source of hemorrhage was identified. The patient therefore underwent gadolinium-enhanced spinal MRI which suggested a possible vascular malformation. A therapeutic laminectomy subsequently confirmed an arteriovenous fistula which was resected. In SS, there are often long delays between symptom onset and definitive diagnosis. Early identification is facilitated by magnetic resonance imaging with gradient-echo sequences. When no source of hemorrhage is identified intracranially, then total spinal cord imaging is indicated to assess for an occult source of hemorrhage as occurred in our case.     

Metronidazole-induced encephalopathy

We report the clinical, neuropsychological, and neuroimaging findings of two patients of diffuse encephalopathy associated with the use of metronidazole. Both patients showed characteristic abnormalities on magnetic resonance imaging (MRI) with diffusion weighted imaging (DWI) and recovered incompletely after the discontinuation of metronidazole. We also suggest that MRI with DWI may be useful in the diagnosis of metronidazole-induced encephalopathy, and that they have a role in the prediction of prognosis.     

Metronidazole neurotoxicity: sequential neuroaxis involvement

Neurological manifestation of metronidazole toxicity include neuropathy and encephalopathy. We report a 67-year-old man with progressive painful paresthesias involving all the four limbs of 3 weeks' duration before admission. He had been treated with metronidazole and cephalosporin for 10 weeks for a hepatic abscess. Five weeks after the symptom onset, he complained of dysarthria and limb ataxia. Magnetic resonance imaging revealed signal abnormalities in the splenium of the corpus callosum and bilateral dentate nuclei. A few hours after brain imaging, the patient exhibited excessive diaphoresis and fluctuation in blood pressure, which resolved within several hours after discontinuation of metronidazole. Whereas his speech returned to near normal within approximately 1 week, a burning sensation was not completely relieved, even 6 months after discharge.     

Reversible metronidazole-induced encephalopathy

We report the neuroimaging findings of a case of reversible metronidazole-induced encephalopathy. Magnetic resonance imaging (MRI) demonstrated lesions in highly suggestive locations. Follow-up imaging performed 1 month after cessation of metronidazole therapy demonstrated resolution of imaging findings.     

Encephalopathy as a predictor of magnetic resonance imaging abnormalities in asphyxiated newborns

Basal ganglia abnormalities on magnetic resonance imaging predict neurodevelopmental impairment in newborns with perinatal depression. We determined the value of a clinical encephalopathy score as a predictor of abnormal magnetic resonance imaging results in newborns with perinatal depression.

We assigned a neonatal encephalopathy score to 101 newborns. The encephalopathy score, based on alertness, feeding, tone, respiratory status, reflexes, and seizure activity, was assigned once daily. The maximum score from the first 3 days of life was compared with abnormal magnetic resonance imaging results present globally or solely in the basal ganglia.

Eighty-one percent of patients manifested abnormalities on any magnetic resonance imaging sequence, and 37% manifested abnormalities in the basal ganglia alone. The encephalopathy score correlated well with magnetic resonance imaging abnormalities in the basal ganglia (Spearman Rho = 0.335, P < 0.0001). Newborns with mild and severe encephalopathy had likelihood ratios of 0.41 and 7.4, respectively, for abnormal basal ganglia magnetic resonance imaging results. Newborns with moderate encephalopathy (composing 47% of the cohort) manifested basal ganglia abnormalities with a likelihood ratio of 0.785.

Severe clinical encephalopathy correlates with abnormal basal ganglia magnetic resonance imaging results, and mild encephalopathy correlates with a normal magnetic resonance imaging result. However, standard clinical criteria do not alter the prior risk of abnormal basal ganglia magnetic resonance imaging results for newborns with moderate encephalopathy.     

Brainstem encephalitis and acute disseminated encephalomyelitis following mumps

A previously healthy female, aged 4 years 3 months, developed brainstem encephalitis with clinical manifestations of fever, decreased level of consciousness, and left facial and abducens paralysis 1 week after bilateral parotitis. Twenty days after remission of encephalitis, she manifested new symptoms of ataxia, dysarthria, and fever. Magnetic resonance imaging revealed multiple hyperintense lesions which were increased in size when compared with the first magnetic resonance imaging. She was treated with glucocorticoids and intravenous immunoglobulin. Forty-eight days after therapy, she was able to walk with support and recovered completely on follow-up. Brainstem encephalitis and acute disseminating encephalomyelitis are discussed as rare complications of mumps.     

Posterior Reversible Encephalopathy and Cerebral Vasoconstriction in a Patient With Hemolytic Uremic Syndrome

BackgroundWe report a patient with hemolytic uremic syndrome who presented with radiological manifestations suggestive of posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome.PatientA 13-year-old girl presented with fever and bloody diarrhea and progressed to develop hemolytic uremic syndrome. She subsequently developed encephalopathy, aphasia, and right-sided weakness.ResultsBrain magnetic resonance imaging showed presence of vasogenic edema in the left frontal lobe, in addition to T2 and fluid-attenuated inversion recovery changes in white matter bilaterally, compatible with posterior reversible encephalopathy syndrome. Magnetic resonance angiography showed beading of the cerebral vessels. Neurological deficits reversed 8 days after symptom onset, with resolution of the beading pattern on follow-up magnetic resonance angiography after 3 weeks, suggesting reversible cerebral vasoconstriction syndrome.ConclusionsBoth posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome may represent manifestations of similar underlying pathophysiologic mechanisms. Recognition of the co-existence of these processes in patients with hemolytic uremic syndrome may aid in judicious management of these patients and avoidance of inappropriate therapeutic interventions.     

A patient with Hashimoto's encephalopathy showing subacute global cognitive dysfunction]

We report a 66-year-old woman with Hashimoto's encephalopathy who showed rapidly developing cognitive deficits, inactivity, and gait disturbance without involuntary movements or convulsions. She had had right-sided hemiparesis and dysarthria caused by a lacunar infarction and had been admitted to our hospital for 2 weeks. Although the dysarthria and hemiparesis gradually improved, difficulty in walking, disorientation, and drowsiness developed 2 months after discharge. Upon readmission, the patient was alert but apathetic and sometimes sleepy. The right upper and lower limbs showed mild weakness, which was considered to be due to the previous infarction. Cerebrospinal fluid showed mild elevation of protein without pleocytosis. An electroencephalogram was normal, and a magnetic resonance imaging of the brain showed only the old lacunar infarction. Titers of antithyroglobulin antibodies and levels of thyroid stimulating hormone in serum were elevated. We made a diagnosis of Hashimoto's encephalopathy and treated the patient with high-dose corticosteroids. Within 1 week, her mental status improved and she was able to walk. Generalized seizure, myoclonus, and tremor, which are characteristic of Hashimoto's encephalopathy, never developed. The findings in this patient suggest that Hashimoto's encephalopathy, a treatable condition, should be included in the differential diagnosis of dementia.     

Pregabalin‐withdrawal encephalopathy and splenial edema: A link to high‐altitude illness?

A postherpetic-neuralgia patient abruptly discontinued pregabalin. Thirty hours later, unexplained nausea, headache, and ataxia developed, progressing to delirium 8 days later. Magnetic resonance imaging indicated T2-hyperintense lesions of her splenium. Similar magnetic resonance imaging abnormalities, interpreted as focal vasogenic edema, develop in some epileptic patients after rapid anticonvulsant withdrawal. Patients with high-altitude cerebral edema have similar splenial-predominant magnetic resonance imaging abnormalities that accompany these same neurological symptoms. This case is the first to associate anticonvulsant-withdrawal splenial abnormalities with neurological symptoms, with gabapentin-type anticonvulsants, and is among the first in nonepileptic patients, suggesting that sudden anticonvulsant withdrawal alone, unaccompanied by seizures, can initiate symptomatic focal brain edema. The similarity of this syndrome to high-altitude cerebral edema suggests a possible common pathophysiology and offers potential therapies.     

Probable variant Creutzfeldt–Jakob disease in Asia: a case report from Taiwan and review of two prior cases

New variant Creutzfeldt–Jakob disease (vCJD) was first identified in the UK in 1996, and was causally linked to bovine spongiform encephalopathy. Herein we report the first case of vCJD in Taiwan: a 34-year-old man who had lived in the UK between 1989 and 1997. The patient presented with depression, irritability, personality change, painful feet and allodynia, followed by gait ataxia and cognitive impairment. Electroencephalograms did not show the typical appearance of sporadic CJD. The cerebrospinal fluid 14-3-3 protein immunoassay was negative. Brain magnetic resonance imaging revealed high signal lesions involving bilateral caudate nuclei, left lentiform nucleus, bilateral dorsomedial thalami and pulvinar on fluid-attenuation inversion recovery, T2- and diffusion-weighted imaging. Prion protein gene analysis showed homozygous for methionine at codon 129. The patient developed akinetic mutism at 16 months and died at 28 months after onset. The clinical presentation and neuroimaging findings were compatible with the vCJD cases reported since 1996, and met the World Health Organization Case Definition for probable vCJD. In this communication, we also review two other cases of vCJD in Asia. All three cases were assumed as imported cases from the UK because of the residential or travel history of the patients.     

Brain Abscess From a Peritonsillar Abscess in an Immunocompetent Child: A Case Report and Review of the Literature

A brain abscess is uncommon but potentially lethal. Common predisposing risk factors include congenital cyanotic heart disease, immunocompromised status, and the presence of septic foci. We describe a left frontal brain abscess accompanied by fever, headache, and weight loss for a 3-month period. The presumptive source of the brain abscess involved a left peritonsillar abscess. To the best of our knowledge, one similar case was reported in the literature in 1929. The specific signs of peritonsillar abscess in our patient included trismus, decreased phonation, and a muffled voice. The peritonsillar abscess was not clinically diagnosed, but incidentally detected on lower axial sections of cranial magnetic resonance imaging. Fever and trismus improved after surgical drainage of the peritonsillar abscess. The cerebral abscess was conservatively treated with intravenous antibiotics. The patient developed hydrocephalus as a sequela to the involvement of the basal meninges.     

海洛因脑病的临床表现与影像学特征

目的:探讨海洛因脑病患者临床表现和影像学特点。方法:回顾性分析经临床和实验室确诊的7例海洛因脑病患者的相关资料。结果:所有患者有吸食海洛因病史,在突然戒断期间中发病,临床以言语障碍,共济失调、锥体束征阳性为特征,MRI表现为对称性大脑、小脑白质、内囊以及脑干的长T1、长T2信号,Gd～DTPA增强后无强化,脑脊液检查一般未见异常。结论:海洛因脑病多见于青年男性,有吸食海洛因史,临床表现多变,影像学有较典型的特点。     

Predictive Value of Neonatal MRI Showing No or Minor Degrees of Brain Injury After Hypothermia

BackgroundMagnetic resonance imaging is a surrogate biomarker for major neurodevelopmental disabilities in survivors of perinatal hypoxic-ischemic encephalopathy because injury to the basal ganglia/thalami is highly predictive of major neuromotor and cognitive problems. Major disabilities and the appearance of neonatal magnetic resonance imaging are improved with therapeutic hypothermia. We evaluated neurodevelopmental outcomes when conventional magnetic resonance imaging showed minimal or no brain injury.MethodsInstitutional review board–approved series of 62 infants (≥36 weeks; ≥1800 g; 34 boys/28 girls) cooled for hypoxic-ischemic encephalopathy between 2005 and 2011 who underwent neonatal magnetic resonance imaging and Bayley Scales of Infant and Toddler Development-III at 22 ± 7 months of age. Magnetic resonance imaging at 5-14 (mean 8) days was scored as normal (score = 0), showing focal gray or white matter injury only (score = 1), or basal ganglia/thalamic and/or watershed lesions with or without more extensive hemispheric injury (score = 2). Sensitivity, specificity, and positive and negative predictive values for magnetic resonance scores 0 and 1 and statistical interaction between magnetic resonance imaging score and age at magnetic resonance imaging were determined.ResultsMagnetic resonance score = 0 was seen in 35/62 patients; 26/35 (74%) were typically developing, seven (20%) had moderate and two (6%) had severe delay. Magnetic resonance score = 1 was seen in 17/62 (27%) patients; 5/17 (29%) were normal, 11/17 (65%) had moderate delay, and 1/17 (6%) had severe neurodevelopmental delay. Of the 52 patients with magnetic resonance scores of 0 and 1, 40% were abnormal. The negative predictive value of a normal magnetic resonance imaging was 74%. For score 1, sensitivity was 95% (confidence interval 63%-83%), specificity 84% (confidence interval 70%-90%), positive predictive value 84% (confidence interval 71%-93%), and negative predictive value 74% (confidence interval 62%-82%).ConclusionsCaution is warranted when prognosticating about neurodevelopmental status in early childhood after hypoxic ischemic encephalopathy with cooling, and longer follow-up studies are needed to determine the prognostic significance of a neonatal magnetic resonance imaging showing no or minor degrees of brain injury.     

Subacute encephalopathy: clinical features, laboratory data, neuroimaging, and outcomes

We sought to clarify the clinical, laboratory, neuroradiologic, and neurophysiologic features of the "subacute" subtype of encephalopathy. We retrospectively identified nine patients with subacute encephalopathy out of 97 patients diagnosed as manifesting acute encephalopathy. Neurologic symptoms, clinical course, laboratory data, neuroradiologic and electroencephalographic findings, and outcomes were reviewed through medical records. The median age of patients was 44 months (range, 28-156 months). The initial neurologic sign was a brief seizure in 4, a prolonged seizure in 3, delirious behavior in 1, and a loss of consciousness in 1. Loss of consciousness the next day was subtle in 4, and mild in 5. However, a worsening of consciousness was observed 3-7 days after onset. Laboratory data were unremarkable, and electroencephalography during the early phase found abnormalities in 4 of 7 patients. Magnetic resonance imaging revealed no abnormalities during the early phase, and mild cortical atrophy during the late phase. All but one patient had various degrees of neurologic sequelae. Subacute encephalopathy was characterized by a delayed worsening of neurologic symptoms, mild cortical atrophy on late magnetic resonance imaging, and poor neurologic outcomes. Recognition of this type of acute encephalopathy is important, and a method to promote early diagnosis is desirable.     

Presumed pituitary abscess without infectious source treated successfully with antibiotics alone.

A 12-year-old girl developed acute frontal headache and severe visual loss in both eyes. A presumptive diagnosis of pituitary abscess was made on the basis of suggestive magnetic resonance imaging findings. These consisted of a large non-enhancing area within the pituitary gland and thin irregular glandular rim enhancement. There was no evidence of pre-existing intracranial or systemic infection. The patient recovered completely after treatment with intravenous and oral antibiotics without surgical drainage. This case highlights the need for a high index of suspicion for pituitary abscess based on unusual imaging findings even when there is no source of infection.