Bilateral Putaminal Necrosis Research Articles

Intracerebral hemorrhage in methanol toxicity patients during COVID-19 pandemic: case report and review of literature.

The aim of this study is to examine the clinical and imaging manifestations of methanol toxicity during the COVID-19 pandemic, as well as to review existing studies on this topic.The most common cause of methanol intoxication is methanol-adulterated liquor. The primary metabolite of methanol, formic acid, is responsible for pathological changes. Symptoms typically present within 6-24h of consumption and can include visual disturbances, acute neurological symptoms, and gastrointestinal issues. During the initial year of the COVID-19 pandemic, methanol poisoning cases increased significantly. In this study, We present six different patients with methanol intoxication and their clinical and imaging features. In the literature review, the most common clinical presentation was loss of consciousness and obtundation and the other was vision loss. CT scan findings showed bilateral putaminal necrosis and hemorrhage in 55% of methanol toxicity patients. Methanol intoxication, causing bilateral putaminal involvement and a 50% mortality rate in intracerebral hemorrhage patients, warrants urgent toxicological analysis due to potential putaminal hemorrhage.

A rare lentiform fork sign in a patient with methanol intoxication with neurological sequelae of parkinsonism and cognitive dysfunction: A case report and literature review

Methanol intoxication is rare in developed countries. Early identification and elimination of the methanol metabolites are vital to an optimal prognosis. A characteristic brain imaging finding is bilateral basal ganglia necrosis and subcortical white matter changes. Here, we report a rare neuroradiological feature called the lentiform fork sign in a patient with methanol intoxication who survived the acute poisoning stage. We report a 31-year-old woman who presented to the emergency department with acute-onset incoherent speech, consciousness disturbance, and a high-anion-gap metabolic acidosis caused by methanol intoxication. She was treated with antidote administration of fomepizole and enhanced methanol elimination through hemodialysis. Neurological sequelae of cognitive decline and parkinsonism developed, with preserved vision. Brain MRI showed bilateral putaminal necrosis and subcortical white matter changes. The apparent diffusion coefficient map showed low signal intensities in the putamen and globus pallidus bilaterally, with brightly hyperintense rims surrounding both putamina that resembled a fork, indicating a lentiform fork sign. She then had sequelae of cognitive decline and delayed parkinsonism feature, which are compatible with the brain lesions on neuroimage studies. Methanol poisoning is an uncommon life-threatening event, and neurological sequelae result from the accumulation of formic acid, a methanol metabolite that inhibits cytochrome c oxidase in mitochondria, leading to neuronal injury. Methanol intoxication should be considered in patients with imaging findings of bilateral basal ganglia necrosis with lentiform fork sign and a metabolic acidosis of unknown origin.

Brain imaging findings of methanol poisoning and detection of chronic stage nervous system damage: A case report

In this article, we presented the chronic neurological findings of an acute case of methanol intoxication due to the use of homemade alcohol. In the neurological examination performed 6 months after intoxication, bilateral vision loss, tremor, dysarthria, dysphagia, loss of taste sensation, and decrease in the Cognitive State Test score were detected. Peripheral polyneuropathy consistent with axonopathy was detected in the peripheral nerve conduction study, and optical neuropathy was detected in the examination of the pattern visual evoked potential. Brain magnetic resonance imaging revealed findings compatible with bilateral putaminal necrosis.

A Case Report of Putaminal Hemorrhage Due to Methanol Toxicity; is Hemodialysis the Offender?

Introduction: Methanol toxicity is a life-threatening condition which is rare in developed countries but common in developing countries. Bilateral putaminal necrosis and hemorrhage are potentially two lethal consequences of methanol toxicity which may be due to direct neurotoxicity of methanol metabolites, especially formic acid, or the consequences of acidosis and hypoxemia in the course of poisoning. Hemodialysis is an important part of the treatment of methanol toxicity and some researchers believe that heparin which is administrated during the hemodialysis may be the cause of putaminal hemorrhage Case report: We report a-32-year old man who presented with acute symptoms of methanol toxicity. A day after hemodialysis he suffered from seizure and Parkinsonism, and the neuroimaging revealed bilateral putaminal hemorrhage. Treatment with Levodopa-carbidopa was introduced for the management of Parkinsonism and finally the patient was discharged with marked improvement of symptoms and relative independency in daily activities Discussion and Conclusion: Our patient suffered from a late manifestation of methanol intoxication, bilateral putaminal hemorrhage, and necrosis. This appearance along with subcortical white matter involvement are the most common abnormalities of methanol toxicity in the brain imaging which can be associated with peripheral enhancement. Based on the reported case and review of present evidences, it is suggested that putaminal hemorrhage in methanol toxicity can be due to anticoagulant agents used in hemodialysis

Visual and neurologic sequelae of methanol poisoning in Saudi Arabia.

Objectives:To present the visual sequelae of methanol poisoning and to emphasize the characteristics of methanol exposure in the Kingdom of Saudi Arabia (KSA).Methods:A retrospective case series was carried out on 50 sequential patients with methanol poisoning seen at the King Khaled Eye Specialist Hospital and King Saud University Hospitals in Riyadh, KSA between 2008 and 2014. All patients were examined by a neuro-ophthalmologist at least one month after methanol intoxication.Results:All 50 patients were young or middle-aged males. All admitted to drinking unbranded alcohol within 2-3 days before profound or relatively profound, painless, bilateral visual loss. Mean visual acuity in this group was hand motions (logMAR 2.82; range 0.1 - 5.0) with some eye to eye variability within individuals. Worse visual acuity was correlated with advancing age (Pearson correlation: oculus dextrus [right eye] - 0.37, p=0.008; oculus sinister [left eye] - 0.36, p=0.011). All patients had optic atrophy bilaterally, and all tested patients had visual field defects. Tremors with or without rigidity were present in 12 patients, and 11 of 30 patients who had neuroimaging performed had evidence of putaminal necrosis.Conclusion:Methanol intoxication causes visual loss within 12-48 hours due to relatively severe, painless, bilateral optic nerve damage that may be somewhat variable between eyes, and is generally worse with advancing age. The coincidence of bilateral optic nerve damage and bilateral putaminal necrosis in a young or middle-aged male is very suspicious for methanol-induced damage.

Rare combination of bilateral putaminal necrosis, optic neuritis, and polyneuropathy in a case of acute methanol intoxication among patients met with hooch tragedy in Gujarat, India

Methanol poisoning is a rare but extremely hazardous form of intoxication, generally occurring after suicidal or accidental events. Methanol is a cheap and potent adulterant of illicit liquors. In India, we have witnessed number of mass emergencies due to adulterated alcohol consumption. Although Gujarat State had banned alcohol consumption since 1961, worse hooch tragedies have often taken place. The most severe consequences of methanol intoxication are blindness, a profound metabolic acidosis and various forms of neurological impairment; which occur characteristically after a latent period of several hours or days after ingestion. We present a unique case of acute methanol intoxication presented with, apart from metabolic acidosis and optic neuritis, involvement of central nervous system and peripheral nervous system. He had bilateral optic neuritis, delayed onset polyneuropathy with axonopathy, and radiculopathy. Magnetic resonance imaging findings were consistent with bilateral putaminal necrosis.

Bilateral Putaminal Necrosis Associated With the Mitochondrial DNA A8344G Myoclonus Epilepsy With Ragged Red Fibers (MERRF) Mutation: An Infantile Case

Myoclonus epilepsy with ragged red fibers (MERRF) is one of the major mitochondrial encephalomyopathies. Its main clinical features are myoclonus epilepsy, ataxia, and myopathy with ragged red fibers. Whereas there is a close correlation between MERRF syndrome and the A8344G mutation of mitochondrial DNA, the reverse is not true. In fact, this mutation is also responsible for various other syndromes, such as Leigh syndrome, spinocerebellar degeneration, atypical Charcot-Marie-Tooth disease, and multiple truncal lipomas. We describe a child with the A8344G mutation of mitochondrial DNA and an unusual clinical, neuroradiologic, and biochemical phenotype, characterized by early-onset, nonprogressive cerebellar ataxia, and subclinical myoclonias in association with bilateral putaminal necrosis on magnetic resonance imaging and a reduction in complex V activity. Our case confirms the existence of a relationship between alteration in adenosine triphosphatase activity and basal ganglia involvement. We recommend that the possibility of a mitochondrial pathology should always be taken into consideration in the presence of bilateral symmetric lesions of the basal ganglia, even when the typical clinical picture is lacking. (J Child Neurol 2006;21:79-82).

Bilateral putaminal necrosis caused by methanol intoxication- A case report

Bilateral putaminal necrosis caused by methanol intoxication- A case report