Neurologic manifestations of diabetic comas: Correlation with biochemical alterations in the brain

Guisado, Raul; Arieff, Allen I.

doi:10.1016/0026-0495(75)90146-8

Cited by 187 publications

(92 citation statements)

References 74 publications

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“…The destruction of the STN causes a decrease of this inhibitory function and increases thalamic excitation of the motor and premotor cortex, resulting in involuntary movement. 12 This mechanism is supported by findings during deep brain stimulation of the subthalamus in Parkinson disease. 13 Possible differential diagnosis in this case includes acute infarction by vascular insult.…”

Section: Discussionmentioning

confidence: 69%

Subthalamic Lesion on MR Imaging in a Patient with Nonketotic Hyperglycemia-Induced Hemiballism: Fig 1.

Kim¹,

Moon²,

Oh³

et al. 2008

AJNR Am J Neuroradiol

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SUMMARY:Hemiballism with corresponding striatal T1 hyperintensity on MR imaging has occasionally been reported in patients with nonketotic hyperglycemia. However, the subthalamic nucleus lesion, which is believed to be pathogenetically related to hemiballism, is rarely documented in a living patient with nonketotic hyperglycemia. We describe a patient with nonketotic hyperglycemia-induced hemiballism, whose responsible lesion (ie, the subthalamus) was demonstrated by MR imaging. Hemiballism-hemichorea (HB-HC) is an involuntary, irregular, wide-amplitude, and poorly patterned movement disorder. HB-HC can mostly result from a focal vascular lesion in the contralateral basal ganglia.1 In the absence of an identifiable focal vascular lesion, metabolic derangements (eg, nonketotic hyperglycemia or hyperthyroidism), brain neoplasm, and infectious diseases of the central nervous system (eg, human immunodeficiency virus infection) are considered to be the more common causes.1 Recent studies have shown that striatal hyperintensity, seen on the T1-weighted MR imaging of the brain, can occur in the acute stage of HB-HC, caused by nonketotic hyperglycemia.2 These radiologic images provided the clue for the early diagnosis of this dyskinesia. Animal studies and subsequent human studies supported the finding that the subthalamus is strongly related to hemiballism.3 There are only scanty reports documenting the subthalamic involvement of nonketotic hyperglycemia in a living patient, which prompted us to report a case of nonketotic hyperglycemia-induced hemiballism, with the responsible subthalamic lesion confirmed by MR imaging. Case ReportA 53-year-old woman was admitted for sudden onset of abnormal movement on the left side. This jerky irregular involuntary movement was first noted on the left leg 3 days before admission. Her symptoms worsened during the last 3 days. She had no history of hypertension, diabetes, headache, parkinsonism, or other neurologic diseases. At admission, her initial blood glucose level was 242 mg/dL and her hemoglobin A 1c concentration was 11.7% (normal values are 70 -110 mg/dL and 4.7-6.4%, respectively). The urine specimen was negative for ketones, indicating nonketotic hyperglycemia. A neurologic examination showed her sensorium to be normal. Deep tendon reflexes were symmetrically hypoactive. The remaining results of the examinations were unremarkable, except for left hemiballism. Brain CT, performed on the first hospital day, revealed no abnormalities. The MR image, obtained 4 days after her initial presentation, showed high signal intensities in the right subthalamic nucleus (STN) on T1-weighted and T2-weighted images (Fig 1) and subtle high signal intensities on diffusion-weighted images (DWIs, not shown). Gradientecho images and B 0 images of DWI showed no susceptibility artifact in the right STN. Contrast-enhanced MR images showed no additional findings. The caudate and putamen appeared normal in all sequences of MR images. Hemiballism was improved with clonazepam (6 mg/day) after 14 days. ...

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Section: Discussionmentioning

confidence: 69%

Subthalamic Lesion on MR Imaging in a Patient with Nonketotic Hyperglycemia-Induced Hemiballism: Fig 1.

Kim¹,

Moon²,

Oh³

et al. 2008

AJNR Am J Neuroradiol

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“…One hypothesis relates to depletion of gamma aminobutyric acid (GABA). 6 In Figure 3 Brain MRI Brain images of patient 2 demonstrate right occipital cortical hyperintensity and subcortical hypointensity on fluidattenuated inversion recovery (A), subtle restricted diffusion in lateral right occipital lobe on diffusion-weighted imaging (B), and marked hypermetabolism of right occipital lobe on FDG-PET (C).…”

Section: Discussionmentioning

confidence: 99%

“…6 The resultant decrease in neuronal GABA leads to proconvulsive activity, even in previously normal brain tissue. This is in contrast to diabetic ketoacidosis, where ketone bodies provide most of the brain energy supply and also convey antiepileptic effect.…”

Section: Discussionmentioning

confidence: 99%

Homonymous hemianopia in nonketotic hyperglycemia is an ictal phenomenon

et al. 2013

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“…In HHS, mental obtundation and coma are more frequent because the majority of patients, by definition, are hyperosmolar (20,141). In some patients with HHS, focal neurological signs (hemiparesis or hemianopsia) and seizures may be the dominant clinical features (141)(142)(143)(144). Although the most common precipitating event is infection, most patients are normothermic or even hypothermic at presentation, because of either skin vasodilation or low fuel-substrate availability.…”

Section: Diagnostic Proceduresmentioning

confidence: 99%

Management of Hyperglycemic Crises in Patients With Diabetes

et al. 2001

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Abbreviations: AaO 2 , alveolar-to-arteriolar oxygen; AKA, alcoholic ketoacidosis; ARDS, adult respiratory distress syndrome; BUN, blood urea nitrogen; CPT, carnitine palmitoyl-transferase; CSF, cerebrospinal fluid; DKA, diabetic ketoacidosis; FFA, free fatty acid; HHS, hyperosmolar hyperglycemic state; IRI, immunoreactive insulin; PaO 2 , arteriolar partial pressure of oxygen; RDKA, recurrent DKA.A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances. Management of Hyperglycemic Crises in Patients With Diabetes T E C H N I C A L R E V I E R e v i e w s / C o m m e n t a r i e s / P o s i t i o n S t a t e m e n t s 132DIABETES CARE, VOLUME 24, NUMBER 1, JANUARY 2001Technical Review noted in newly diagnosed obese type 2 diabetic patients (5,26,31). Therefore, the concept that the presence of DKA in type 2 diabetes is a rare occurrence is incorrect.The most common types of infections are pneumonia and urinary tract infection, accounting for 30-50% of cases (Table 4). Other acute medical illnesses as precipitating causes include alcohol abuse, trauma, pulmonary embolism, and myocardial infarction, which can occur both in type 1 and 2 diabetes (6). Various drugs that alter carbohydrate metabolism, such as corticosteroids, pentamidine, sympathomimetic agents, and ␣-and ␤-adrenergic blockers, and excessive use of diuretics in the elderly may also precipitate the development of DKA and HHS.The recent increased use of continuous subcutaneous insulin infusion pumps that use small amounts of short-acting insulin has been associated with an incidence of DKA that is significantly increased over the incidence seen with conventional methods of multiple daily insulin injections, in spite of the fact that most of the mechanical problems with insulin pumps have been resolved (6,(32)(33)(34). In the Diabetes Control and Complications Trial, the incidence of DKA in patients on insulin pumps was about twofold higher than that in the multipleinjection group over a comparable time period (35). This may be due to the exclusive use of short-acting insulin in the pump, which if interrupted leaves no reservoir of insulin for blood glucose control.Psychological factors and poor compliance, leading to omission of insulin therapy, are important precipitating factors for recurrent ketoacidosis. In young female patients with type 1 diabetes, psychological problems complicated by eating disorders may be contributing factors in up to 20% of cases of recurrent ketoacidosis (36,37). Factors that may lead to insulin omission in younger patients include fear of weight gain with good metabolic control, fear of hypoglycemia, rebellion against authority, and stress related to chronic disease (36). Noncompliance with insulin therapy has been found to be the leading precipitating cause for DKA in urban African-Americans and medically indigent patients (5,26). In addition, a recent study showed that diabetic patients without health insurance or with Medicaid alone had hospitali...

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Neurologic manifestations of diabetic comas: Correlation with biochemical alterations in the brain

Cited by 187 publications

References 74 publications

Subthalamic Lesion on MR Imaging in a Patient with Nonketotic Hyperglycemia-Induced Hemiballism: Fig 1.

Subthalamic Lesion on MR Imaging in a Patient with Nonketotic Hyperglycemia-Induced Hemiballism: Fig 1.

Homonymous hemianopia in nonketotic hyperglycemia is an ictal phenomenon

Management of Hyperglycemic Crises in Patients With Diabetes

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