Acessibilidade / Reportar erro

Intoxication with oral hypoglycemics as a cause of diffuse brain injury: case report

Intoxicação com hipoglicemiante oral como causa de lesão cerebral difusa: relato de caso

Abstracts

OBJECTIVE: To present the imaging findings of a patient with diffuse brain injury secondary to intoxication with oral hypoglycemics. CASE REPORT: A nine years-old boy presented with generalized tonic-clonic convulsions and decreased consciousness. Laboratory investigation demonstrated blood glucose level of 21 mg/dL. The magnetic resonance imaging showed cortical and subcortical temporo-parieto-occipital areas of high signal on T2 and low signal on T1, with high signal on the diffusion-weighted images and low signal on apparent diffusion coefficient maps. CONCLUSION: Cortical and subcortical temporal, parietal and occipital ischemic lesions may be seen in patients with intoxication by oral hypoglycemics.

magnetic resonance imaging; diffusion weighted imaging; hypoglycemia


OBJETIVO: Apresentar os achados de imagem em um caso de lesão cerebral difusa secundária a intoxicação por hipoglicemiante oral. RELATO DE CASO: Menino de nove anos de idade apresentando crises convulsivas tônico-clônicas e rebaixamento do nível de consciência. Exames laboratoriais revelaram glicose sérica de 21 mg/dL. O exame de ressonância magnética revelou lesões corticais e subcorticais têmporoparieto-occipitais, com alto sinal em T2 e baixo em T1, apresentando hipersinal nas imagens ponderadas em difusão e hipossinal nos mapas de coeficiente aparente de difusão. CONCLUSÃO: Lesões isquêmicas corticais e subcorticais nos lobos temporais, parietais e occipitais podem ser identificadas em pacientes com intoxicação por hipoglicemiantes orais.

ressonância magnética; imagens ponderadas em difusão; hipoglicemia


Intoxication with oral hypoglycemics as a cause of diffuse brain injury: case report

Intoxicação com hipoglicemiante oral como causa de lesão cerebral difusa: relato de caso

Emerson L. Gasparetto; Leila Caroline Bianchet; Taisa Davaus; Arnolfo de Carvalho Neto

Discipline of Diagnostic Radiology, Department of Internal Medicine, University of Paraná (ELG, JMR, TD, ACN) and DAPI - Diagnóstico Avançado Por Imagem (ACN), Curitiba PR, Brazil

ABSTRACT

OBJECTIVE: To present the imaging findings of a patient with diffuse brain injury secondary to intoxication with oral hypoglycemics.

CASE REPORT: A nine years-old boy presented with generalized tonic-clonic convulsions and decreased consciousness. Laboratory investigation demonstrated blood glucose level of 21 mg/dL. The magnetic resonance imaging showed cortical and subcortical temporo-parieto-occipital areas of high signal on T2 and low signal on T1, with high signal on the diffusion-weighted images and low signal on apparent diffusion coefficient maps.

CONCLUSION: Cortical and subcortical temporal, parietal and occipital ischemic lesions may be seen in patients with intoxication by oral hypoglycemics.

Key words: magnetic resonance imaging, diffusion weighted imaging, hypoglycemia.

RESUMO

OBJETIVO: Apresentar os achados de imagem em um caso de lesão cerebral difusa secundária a intoxicação por hipoglicemiante oral.

RELATO DE CASO: Menino de nove anos de idade apresentando crises convulsivas tônico-clônicas e rebaixamento do nível de consciência. Exames laboratoriais revelaram glicose sérica de 21 mg/dL. O exame de ressonância magnética revelou lesões corticais e subcorticais têmporoparieto-occipitais, com alto sinal em T2 e baixo em T1, apresentando hipersinal nas imagens ponderadas em difusão e hipossinal nos mapas de coeficiente aparente de difusão.

CONCLUSÃO: Lesões isquêmicas corticais e subcorticais nos lobos temporais, parietais e occipitais podem ser identificadas em pacientes com intoxicação por hipoglicemiantes orais.

Palavras-chave: ressonância magnética, imagens ponderadas em difusão, hipoglicemia.

Diffuse brain injury are caused by several disorders, such as hypoglycemia. In addition, different conditions may cause hypoglycemia. In neonates, the most common causes are maladaptive metabolic adjustments in the transition intrauterine to extra uterine life, intrauterine under nutrition, and primary enzymatic or metabolic endocrine abnormalities. Considering another ages, exogenous intoxication and hypoxic-ischemic disorders are the causes of hypoglycemia most frequently demonstrated1,2. The histopathological findings seen in patients with transient hypoglycemia and diffuse brain injury have been documented. However, there are only a few studies stressing the imaging findings in these patients1-4. Barkovich et al.2, reviewed the imaging findings of five patients with transient neonatal hypoglycemia. The most common feature was diffuse cortical and subcortical white matter damage, with the parietal and occipital lobes being affected more severely. Globus pallidus injury was seen only in one patient, who had the most severe cortical injury. The diffusion-weighted image (DWI) is a neuroimaging technique that evaluates the water movement, detecting the tissue injury as in acute cerebral damages. Singhal et al.5 demonstrated the DWI features in three patients who suffered different conditions of anoxic brain injury. All the cases showed severe diffuse lesions in the gray matter of the parietal and occipital lobes, as well as in the striatum, thalamus and hippocampus. To our knowledge, the DWI findings in patients with brain lesions secondary to severe hypoglycemia have not been reported.

We present the imaging findings of a patient with diffuse brain injury secondary to intoxication with oral hypoglycemics, emphasizing the DWI features.

CASE

A previously healthy nine years old boy was admitted to the hospital with generalized tonic-clonic convulsions and decreased consciousness. His grandmother informed that he had cough and nasal congestion in the two days before, and she gave him some analgesics. At the physical examination he was comatose and showed left ocular deviation. Laboratory investigation demonstrated blood glucose level of 21 mg/dL. Immediately it was administered a bolus of 10% glucose followed by rapid drip infusion. The glucose levels increased to 44 mg/dL after six hours, when he was admitted at the Intensive Care Unit (ICU) and started anti-convulsive drugs (hydantol and benzodiazepines). Another laboratory results were unremarkable. At that time, head CT scan was normal.

At ICU the glucose blood levels were progressively corrected. In the following days, the electroencephalogram showed diffuse slowly of base activity and outbreaks of generalized irritative activities in brain hemispheres. The patient underwent head CT scan, which demonstrated multiple hypodense subcortical areas in the temporal, parietal and occipital lobes. The MRI showed cortical and subcortical areas of high signal on T2-weighted images and discrete low signal on T1-weighted images at the same regions demonstrated in the CT scan (Fig A-B). These areas demonstrated high signal on the DWI and low signal on apparent diffusion coefficient (ADC) maps, suggesting an acute ischemic event.


The grandmother was asked to show the analgesics that the child had ingested, and, actually, they are tablets of oral hypoglycemics that she was taking for diabetics. The patient progressively recovered the consciousness level and discharged the hospital two months later with mild cognition deficit and motor deficiency and some episodes of seizures. On the follow-up, four months later, the patient was showing hyporeflexia in the lower extremity, stereognosis and mild motor incoordination. At this time, the parents agreed with the publication of the case and signed the consent.

DISCUSSION

Hypoglycemia, as a cause of diffuse brain injury, can determine characteristic patterns of damage according to the duration of the event, and patient’s age. Maladaptative metabolic adjustments during the transition intrauterine to extra uterine life, intrauterine under nutrition, secondarily to specific primary enzymatic or metabolic endocrine abnormalities are the main causes of hypoglycemia in neonates2. Exogenous intoxication, as seen in this case, and hypoxic ischemic disorders are the main causes of hypoglycemia in another ages.

Neuroimaging studies emphasizing the distribution of brain injury in patients with hypoglycemia may evidence a disproportionate involvement of the parietal and occipital lobes1-6. Spart et al.1 showed the CT and MRI findings of one patient with severe hypoglycemia and found progressive parenchymal loss with predominant occipital involvement. Abnormally high intensity in periventricular deep white matter of parieto-occipital lobes on T2-weighted images and hypointensity on T1-weighted were considered characteristic patterns of hypoglycemic lesions7.

The diffusion-weighted MRI is based on the free movement of the water molecules along random pathways (Brownian motion). Usually, water protons diffuse within a tissue and apparent rate and direction of this diffusion will reflect the barriers that these protons undergo during its translational path length. The diffusion technique uses a pair of gradient pulses to diphase and subsequently rephase protons. Protons experiencing slow or hindered diffusion will largely rephase and it will appear as retention of high signal intensity. Nowadays, there are many applications of DWI in neuroimaging8,9. Besides, helping to differentiate acute from chronic infarction in patients with cerebral ischemia still is the main application of the technique5,6.

In this case, initial head CT scan was normal. Subsequently, the CT scan showed multiple hypodense subcortical areas in the temporal, parietal and occipital lobes. In addition, the MRI demonstrated cortical and subcortical areas of high signal on T2-weighted images and discrete low signal on T1-weighted images at the same regions demonstrated in the CT scan. In these regions the DWI demonstrated high signal and ACD maps low signal, suggesting acute ischemia.

In conclusion, patients with severe hypoglycemia secondary to oral intoxication may present a pattern of diffuse brain damage, showing in the MRI cortical and subcortical temporo-parieto-occipital areas of low signal on T1- and high signal on T2-weighted images. In addition, the DWI may show signals of restriction of the water movement in these areas, allowing the early diagnosis of this severe cause of brain injury.

Received 22 February 2006, received in final form 20 July 2006. Accepted 6 September 2006.

Dr. Arnolfo de Carvalho Neto - DAPI - Diagnóstico Avançado Por Imagem - Rua Brigadeiro Franco 122 - 80430-210 Curitiba PR - Brasil. E-mail: arnolfocarvalho@hotmail.com

  • 1. Cakmakci H, Usal C, Karabay N, Kovanlikaya A. Transient neonatal hypoglycemia: cranial US and MRI findings. Eur Radiol 2001;11: 2585-2588.
  • 2. Barkovich JA, Ali Al F, Rowley H, Bass N. Imaging patterns of neonatal hypoglycemia. AJNR Am J Neuroradiol 1998;19:523-528.
  • 3. Rutherford M. Whats new in neuroimaging? Magnetic resonance imaging of the immature brain. Eur J Pediatric Neurol 2002;6:5-13.
  • 4. Muramaki Y, Yamashita Y, Matsuishi T, Utsunomiya H, Okudera T, Hashimoto T. Cranial MRI of neurologically impaired children suffering from neonatal hypoglycemia. Pediatr Radiol 1999;29:23-27.
  • 5. Els T, Kassubeck J, Kubalek R, Klisch J. Diffusion-weighted MRI during early global cerebral hypoxia: a prediction for clinical outcome? Acta Neurol Scand 2004;110:361-367.
  • 6. Singhal A, Topruoglu M, Koroshetz W. Diffusion MRI in three types of anoxic encephalopathy. J Neurol Sci 2002;196:37-40.
  • 7. Caraballo R, Sakr D, Mozzi M, et al. Symptomatic occipital lobe epilepsy following neonatal hypoglycemia. Pediatric Neurol 224;31:24-29.
  • 8. Toichi T, Kira R, Takemoto M, et al. Diagnostic usefulness of diffusion-weighted magnetic resonance imaging in influenza-associated acute encephalopathy or encephalitis. Brain Dev 2000;22:451-453.
  • 9. Roelants-van M, Nikkels G, Groenendaal F, et al. Neonatal diffusion-weighted MR imaging: relation with histopathology or follow-up MR examination. Neuropediatrics 2001;32:286-294.

Publication Dates

  • Publication in this collection
    21 Dec 2006
  • Date of issue
    Dec 2006

History

  • Reviewed
    20 July 2006
  • Received
    22 Feb 2006
  • Accepted
    06 Sept 2006
Academia Brasileira de Neurologia - ABNEURO R. Vergueiro, 1353 sl.1404 - Ed. Top Towers Offices Torre Norte, 04101-000 São Paulo SP Brazil, Tel.: +55 11 5084-9463 | +55 11 5083-3876 - São Paulo - SP - Brazil
E-mail: revista.arquivos@abneuro.org