Neuroimaging of toxic and metabolic disorders

Imaging of the brain, magnetic resonance imaging (MRI) in particular, is a key adjunctive tool in the diagnosis and management of toxic-metabolic disorders such as alcoholism, mitochondrial encephalopathies, disorders of iron or copper metabolism, exposure to carbon monoxide, radiotherapy, immunosuppressive agents, toluene, and recreational drugs. In this article, we review the neuroimaging findings of common toxic and metabolic disorders focusing on the role of conventional MRI. We also consider advanced imaging methods, such as magnetic resonance spectroscopy, diffusion MRI, and positron emission tomography. We hope this article will prove useful to trainees and practitioners in the clinical and imaging fields of the neurosciences.     

High-Resolution Magnetic Resonance Imaging Reveals Symmetric Bitemporal Cortical Necrosis After Carbon Monoxide Intoxication

High-resolution magnetic resonance images obtained in a patient several months after carbon monoxide (CO) intoxication revealed nearly symmetric regional atrophy of both lateral temporal lobes. This pattern of cortical lesions after CO exposure has not been reported before. The patient suffered from severe cognitive deficits including a transient Klüver-Bucy-like behavior. This report underlines the value of high-resolution magnetic resonance imaging in chronic stages of CO intoxication in the attempt to understand the neuroanatomical bases of the observed behavior.     

Neurologic and radiologic manifestations of three girls surviving acute carbon monoxide poisoning

We report the neurologic and radiologic manifestations of three adolescent girls with acute carbon monoxide poisoning. The girls were found collapsed and unconscious in a bathroom where liquid petroleum gas was being used as heating fuel. As hyperbaric oxygen therapy was not available locally, they only received oxygen supplementation via nasal cannula (4 L/minute) as treatment in the first 2 days. On transfer to a tertiary center in Hong Kong, evolving neurologic manifestations of visual acuity and field deficits, confusion, and focal motor weaknesses were observed. Focal infarctions were evident in cerebral computed tomography in one patient and cortical lesions on magnetic resonance imaging in all three patients. [18F]Fluorodeoxyglucose (FDG) positron emission tomography (PET) revealed additional decreased metabolism in the basal ganglia in two patients, which was typical of carbon monoxide poisoning. The neurologic deficits resolved completely at 3 weeks after the exposure, but psychologic symptoms succeeded. This report serves to alert clinicians to the varied neuro-ophthalmologic manifestations and psychologic impairment even with the same duration of carbon monoxide poisoning. PET might be more sensitive in detecting cerebral injuries specific for carbon monoxide poisoning.     

Delayed neurological deterioration following carbon monoxide poisoning: MRI findings

We present two patients with delayed neurological deterioration following apparent recovery from carbon monoxide poisoning in whom magnetic resonance imaging showed abnormalities. In the first patient, cortical grey matter abnormalities were seen without white matter changes. Visual evoked potentials were, however, abnormal. In the second, diffuse white matter lesions were detected. In neither patient were basal ganglia lesions seen.     

A case of carbon monoxide intoxication presenting subacute dementia as the initial symptom]

We reported a 67-year-old woman who had developed abnormal behavior and dementia from January 21, 2001 and deteriorated to akinetic mutism on February 15. T2-weighted magnetic resonance imaging showed high intensity in bilateral globus pallidus and a rapid spreading of diffuse high intensity in bilateral deep white matter. Later on, we got an important information that she had used a little coal stove three times about three weeks before presenting the initial symptom. She was diagnosed as carbon monoxide intoxication and treated with hyperbaric oxygen from March 1. A remarkable improvement on dementia and motor disability was observed. We conclude that this case is the first reported example of a case of intermittent carbon monoxide intoxication presenting subacute dementia as an initial symptom.     

Magnetic Resonance Imaging Findings on Carbon Monoxide Intoxication

Four patients who had carbon monoxide intoxication were examined by brain magnetic resonance imaging (MRI) and computed tomography (CT). Three were unconscious in the acute stage of intoxication. On regaining consciousness. neuropsychological symptoms and signs remained. In these patients, T2-weighted MRI demonstrated hyperintensity lesions in the cerebral cortex, most prominent in the watershed zone. The fourth patient had only memory disturbance and was not unconscious during the acute intoxication. The T1-weighted MRI showed hyperintensity in the bilateral pallidal regions. MRI demonstrated lesions more clearly than did CT.     

Chronic exposure to carbon monoxide in two elderly patients using a kotatsu,a traditional Japanese charcoal‐based heater

We report on two elderly patients with cognitive impairments, for whom chronic carbon monoxide (CO) exposure was suspected based on elevated carboxyhaemoglobin levels in their serum. On their initial visits, cognitive impairment and brain magnetic resonance imaging findings in both patients were compatible with the diagnosis of Alzheimer's‐type dementia. However, after discontinuation of the use of a kotatsu, a charcoal‐based heater, their serum carboxyhaemoglobin levels normalized and their physical symptoms resolved. Their cognitive function also slightly improved. The causal relationship between physical symptoms and cognitive impairment after chronic CO poisoning is uncertain; however, it is possible that chronic exposure to low CO levels exacerbated the clinical manifestation in our patients.     

A case of adult onset tic disorder following carbon monoxide intoxication

BACKGROUND: Adult onset tic disorders are usually secondary in origin. We report a case of adult onset tic disorder following carbon monoxide (CO) intoxication with typical magnetic resonance imaging features. CASE REPORT: A 36-year-old woman developed temporarily suppressible patterned movements on her face, neck, and shoulder associated with sensory discomfort after CO poisoning. Magnetic resonance images showed bilateral symmetric cavitary changes in the globus pallidus. Clonazepam relieved much of her symptoms. CONCLUSION: Our patient developed a monosymptomatic tic disorder following CO intoxication. This further supports that altered outflow signals from the basal ganglia, especially the globus pallidus, may contribute to the development of tic disorders.     

Carbon monoxide poisoning: clinical,neurophysiological, and brain imaging observations in acute disease and follow-up

Summary Five patients (aged 19–52 years) were treated for a midbrain syndrome due to acute carbon monoxide poisoning and had clinical follow-up investigations for up to 18 months. Three patients recovered with minor neurological and neuropsychological deficits and resumed their premorbid life-style. One patient had normal findings, while the fifth remained in a permanent vegetative state. Initial CT of the brain may fail to detect low-density lesions in the globus pallidus. If present, these lesions may either have disappeared, diminished, or remained unchanged at follow-up. Long-term outcome seems to show a closer link to white matter changes, which are at present best investigated by magnetic resonance imaging. The additional value of determining visual evoked responses at repeated follow-up is suggested by the present investigation.     

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.     

Magnetic resonance imaging in the evaluation of intracranial hemorrhage

Magnetic resonance imaging is emerging as a valuable tool for the urgent evaluation of patients with acute stroke. This review focuses on the applications of magnetic resonance imaging in the diagnosis and management of intracranial hemorrhage. The biophysical properties of blood in the neuroaxis and the magnetic resonance imaging evolution of intracranial bleeding are reviewed. The potential applications of magnetic resonance imaging in the evaluation and therapy of specific types of intracranial hemorrhage are discussed. Emphasis is made on the superiority of magnetic resonance imaging in detecting intracranial hemorrhage and ischemic stroke. Although there is some hesitation to perform magnetic resonance imaging to evaluate acute intracranial hemorrhage, there is strong evidence that magnetic resonance imaging is not inferior to computerized tomography in this clinical setting. In the era of acute stroke intervention, magnetic resonance imaging offers significant advantages over computed tomography.     

Digit and letter alexia in carbon monoxide poisoning

This study examined a 24-year-old patient with delayed encephalopathy, who was admitted to hospital with complaints of headache and visual impairment 1 week after acute carbon monoxide poisoning. The results of a visual field assessment, electroencephalography and head magnetic resonance imaging indicated damage to the cerebral cortex. After a 2-week treatment period, the patient had recovered from the visual impairment, but exhibited digit- and letter-reading difficulty. The Chinese aphasia battery and the number and letter battery supplement were conducted. The results revealed that the patient exhibited digit and letter alexia, while the ability to read Chinese characters was preserved. In contrast, the patient exhibited a deficit in Chinese character writing, while number and letter writing remained intact. Following treatment, reading and writing ability was improved and electroencephalographic abnormalities were ameliorated. Overall, our experimental findings demonstrated that delayed encephalopathy following acute carbon monoxide poisoning was characterized by digit and letter alexia.     

Multiple sclerosis disease activity correlates with gadolinium-enhanced magnetic resonance imaging

Magnetic resonance imaging provides a method of visualizing multiple sclerosis plaques, but the age and activity of these plaques cannot be determined with routine magnetic resonance images. Gadolinium DTPA is a paramagnetic contrast agent that does not cross an intact blood-brain barrier. We studied 16 patients with multiple sclerosis, using magnetic resonance imaging, gadolinium-enhanced magnetic resonance imaging, and computed tomographic scans. Gadolinium enhancement of multiple sclerosis plaques correlated with the clinical activity of the disease and corresponded anatomically with the symptoms and signs. We conclude that gadolinium enhancement of magnetic resonance images is a promising tool in the investigation of multiple sclerosis lesions and that it may provide a method for objective follow-up in clinical trails.     

A case of delayed postanoxic encephalopathy with bilateral lesions of the corpus striatum

Delayed neurological deterioration following anoxia is known to result from carbon monoxide exposure. However, it may also occur with anoxia of other types as well. The present report describes a case of delayed postanoxic encephalopathy with bilateral striatal lesions demonstrated by magnetic resonance imaging. A 27-year-old man exhibited anoxic anoxia caused by upper airway obstruction following general anesthesia for shoulder fracture surgery. Initially he was delirious and markedly excited for one day and became apparently normal for the following three days. Then he relapsed into delayed neurological deterioration with speech and gait disturbance, clumsiness of hand, pyramidal signs and metamorphopsia. Thereafter, he became bed-ridden and fell into semicomatose state with marked motor restlessness, involuntary movement of the tongue and decorticate posture. Twenty-five days later he had a second recovery period after hyperbaric oxygenation that lead to the sequelae with speech and motor disturbances and mild mental changes. I examined the present case as an expert witness in a civil suit eleven years after initial anoxia. The patient showed slight intellectual impairment and personality change. Impairment in figure-ground differentiation and disorders of spatial thought were also observed. Neurological examination revealed anisocoria, dysarthria with acquired stuttering, disturbances of fractionated movement of fingers, writer's cramp and Babinski's sign bilaterally. Postural dystonia of both hands and fingers, rigidity and spasticity of all extremities were also present. Magnetic resonance imaging (MRI) showed bilateral lesions of the corpus striatum, especially of the putamen. Some portion of the caudate nucleus was also involved. Cerebral cortices and white matter were slightly atrophic. From the above clinical course and neurological findings, we diagnosed the present case as delayed postanoxic encephalopathy. Ginsberg (1979) noted that in cases of anoxia not related to carbon monoxide, diffuse demyelinative changes of cerebral hemispheral white matter tended to be associated with relapsing clinical course, and gray matter injury was only seen in a few cases. MRI findings in the present case suggest that main site of the lesion to be in gray matter of the corpus striatum. In this respect, the present case is considered to be noteworthy.     

Diffusion tensor magnetic resonance imaging tractography in cognitive disorders

PURPOSE OF REVIEW: The advent of novel techniques for tracing connections in vivo, such as diffusion tensor magnetic resonance imaging tractography, allows us, for the first time in the human brain, to study the microstructural integrity of white matter fibres and perform virtual dissections of large scale neurocognitive networks. This review will outline the advantages and limitations of applying diffusion tensor magnetic resonance imaging to the study of cognitive and behavioural disorders in neurology and psychiatry. RECENT FINDINGS: Diffusion tensor magnetic resonance imaging has been used to re-explore the anatomy of white matter tracts in the living human brain and to create connectional models of brain function. Beyond its application to classical disconnection syndromes, diffusion tensor magnetic resonance imaging is becoming an important tool to extend the disconnectionist paradigm to neurodevelopmental and neurodegenerative disorders. SUMMARY: For the first time, we are able to correlate disconnecting lesions with clinical symptoms in vivo and test the disconnection mechanism directly in cognitive disorders. With diffusion tensor magnetic resonance imaging tractography alone and in combination with other magnetic resonance imaging techniques, researchers are able to detect abnormalities in white matter that are not visible with conventional magnetic resonance imaging.     

Parkinsonism, pyramidal signs, polyneuropathy, and cognitive decline after long-term occupational solvent exposure

It is well known that exposure to manganese, solvents, or carbon monoxide in an occupational setting may lead to central nervous system damage and parkinsonism. The most important solvents in this respect are methanol, toluene, carbon disulfide, and n-hexane. We describe three patients who had been exposed to various solvents for more than 20 years (25, 34, and 46 years). They presented with parkinsonism, pyramidal signs, mild cognitive decline, and unresponsiveness to levodopa. Two patients had a predominantly axonal and sensory polyneuropathy of the lower legs with fasciculations in one of them. Parkinsonian features were progressive, even after the patients had stopped work. We present clinical data, neuropsychological findings, and results of brain computed tomography or magnetic resonance imaging, electroneuromyography, evoked potentials, single photon emission computed tomography, and positron-emission tomography. There is growing evidence that various organic solvents give rise to a parkinsonism syndrome with pyramidal features in susceptible individuals. Received: 22 December 1997 Receibed in revised form: 17 July 1998 Accepted 21 July 1998     

Unexplained neurological events during bathing in young people: Possible association with the use of gas geysers

Here, we report sudden, unexplained neurological collapse in 14 young people while bathing with hot water associated with the use of liquefied petroleum gas (LPG)-based water heaters (gas geysers) in ill-ventilated bathrooms. None of the patients reported any circumstantial evidence of seizures or prior epilepsy. One patient developed cortical blindness and demonstrated posterior leucoencephalopathy on imaging studies. The remaining patients made rapid and excellent recovery without any residual neurological sequelae. In these cases, the results of all routine investigations, i.e., serum chemistry, brain imaging (computed tomography in 2 and magnetic resonance imaging in 10) and electroencephalography were normal. The clinical clustering of these cases in winter months with similar presentations of reversible encephalopathy probably indicates an inhalational toxin exposure. Therefore, we postulate a hypothesis that harmful emissions consisting of carbon monoxide (CO), hydrocarbon gases (HC) and nitrogen oxides (NOx), produced by incomplete combustion of LPG might be responsible for the cellular injury and subsequent transient neurological deficits. Physicians should be aware of this entity in order to avoid misdiagnosis of this condition as seizures, and a public awareness should also be created regarding the proper use of these devices.     

Magnetic resonance imaging detection of mesial temporal sclerosis in children

The objective of this study was to investigate the prevalence and clinical characteristics of mesial temporal sclerosis as diagnosed by brain magnetic resonance imaging in children. A total of 390 consecutive brain magnetic resonance imaging studies in children were reviewed for evidence of mesial temporal sclerosis. Subsequently, the magnetic resonance imaging scans and charts of patients with mesial temporal sclerosis were reviewed and their clinical details were evaluated. The magnetic resonance imaging studies had been performed for multiple indications, including seizures, headache, and developmental problems. In children, the prevalence of mesial temporal sclerosis among all brain magnetic resonance imaging studies was 3.1% (12 of 390 studies) and 12.1% (12 of 99 studies) among all brain magnetic resonance imaging studies performed for seizures. These children all presented with a history of seizure disorder, often had other medical problems, and histopathology (when available) nearly always (5 of 6 patients) confirmed their magnetic resonance imaging diagnosis of mesial temporal sclerosis. The prevalence of mesial temporal sclerosis is low among all pediatric patients who had magnetic resonance imaging brain studies. All our mesial temporal sclerosis patients had clinical seizures; i.e., it was never an "incidental finding". Children with mesial temporal sclerosis often had comorbid conditions, and the diagnosis of mesial temporal sclerosis made by magnetic resonance imaging was accurate when compared with the available histopathology.     

MRI follow-up of basal ganglia involvement in subacute sclerosing panencephalitis

A 12-year-old male with subacute sclerosing panencephalitis is presented. Magnetic resonance imaging revealed basal ganglia involvement without white matter changes for several months. Basal ganglia changes are not infrequent in subacute sclerosing panencephalitis, but they tend to appear in advanced clinical stages. Prominent basal ganglia involvement may occur very rarely in subacute sclerosing panencephalitis. In our patient, serial magnetic resonance imaging demonstrated the involvement of white matter after 2 years of magnetic resonance imaging follow-up. In contrast with the neuroradiologic progression, our patient’s clinical status remained stable.     

The brain lesion responsible for parkinsonism after carbon monoxide poisoning

BACKGROUND: Parkinsonism is a common neurological sequela of carbon monoxide (CO) poisoning, but its pathophysiological mechanism has yet to be clarified. OBJECTIVES: To describe a married couple who were both affected by CO poisoning, but only 1 of whom developed CO-induced parkinsonism, and to discuss the possible underlying pathophysiological mechanism of CO-induced parkinsonism by comparing the neuroimaging findings of these patients. DESIGN AND SETTING: Case report from a clinical neurology department. PATIENTS: A married couple experienced CO poisoning simultaneously. One month later, only the husband gradually developed delayed sequelae, including parkinsonism and intellectual impairment. On detailed neurological examination, the husband showed mild but definite rigidity and bradykinesia, while no parkinsonian signs were observed in the wife. Neuropsychological examination revealed impaired memory and attention in both patients, but they were more severe in the husband than in the wife. Magnetic resonance imaging scans of the patients' brains disclosed diffuse high-intensity white matter signals in both patients and bilateral pallidal necrosis in the wife. Dopamine transporter imaging showed that the degree of dopamine neuronal loss was comparable between these patients. Magnetic resonance spectroscopy revealed more severe white matter damage in the husband than in the wife. Thirteen months later, neurological and neuropsychological examinations showed complete recovery from parkinsonism as well as intellectual impairment. Follow-up magnetic resonance spectroscopy also suggested remarkable improvements in white matter damage. CONCLUSION: These results support the role of white matter damage in producing parkinsonism after CO poisoning and highlight the possible usefulness of magnetic resonance spectroscopy in predicting delayed sequelae in patients after CO poisoning. Arch Neurol. 2000;57:1214-1218