1/16. Blood brain barrier destruction in hyperglycemic chorea in a patient with poorly controlled diabetes.A case of hemichorea in a patient with poorly controlled diabetes is reported. T1-weighted magnetic resonance imaging (MRI) showed an unusual homogeneous high-intensity area in the corpus striatum. Of interest in the case was the fact that the globus pallidus, which was enhanced with gadolinium at the onset of hemichorea, showed homogeneous high-intensity on a subsequent T1-weighted image. This indicated that blood brain barrier destruction preceded the signal intensity change in the basal ganglia. As far as the authors could determine, this is the first reported case showing such enhancement during the course of diabetic hemichorea.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
2/16. Non-ketotic hyperglycemia in a young woman, presenting as hemiballism-hemichorea.We report a 22-year-old girl presenting with acute onset left sided hemiballism-hemichorea (HH) and non-ketotic hyperglycemia (NKH). Initial brain CT revealed faint hyperdensities, sharply confined to the contralateral nucleus caudatus and putamen. Sequential MRI investigations yielded increasing hypersignal intensities on T1-weighted images and resolving hypodensities on T2-weighted images of the right striatum, leaving small sequelae in the head of the right caudate nucleus. NKH is an unusual cause of HH. The abnormalities seen in neuroimaging are rare, but seem to be quite specific to this syndrome. We give an update on current literature regarding the possible pathophysiological processes underlying this specific clinical entity.- - - - - - - - - - ranking = 0.2keywords = brain (Clic here for more details about this article) |
3/16. Presentation of striatal hyperintensity on T1-weighted MRI in patients with hemiballism-hemichorea caused by non-ketotic hyperglycemia: report of seven new cases and a review of literature.Recent studies have shown unique clinicoradiologic characteristics in patients with hemiballism-hemichorea (HB-HC) caused by non-ketotic hyperglycemia; however, there is still a limited number of patients being reported. We report 7 patients (3 males and 4 females) with this type of dyskinesia, whose ages ranged from 60 to 84 years. Brain CT of these patients showed hyperdensity in the contralateral striatum, corresponding with MRI studies that showed an increased signal intensity on T1-weighted images and a decreased signal on T2-weighted images. After metabolic control had been achieved, the hyperkinetic state of these patients abruptly ceased. Follow-up neuroimaging studies in 2 patients documentied complete resolution of the striatal hyperintensity on brain CT and MRI after 3 months and 6 months, respectively. A review of patients with HB-HC caused by non-ketotic hyperglycemia reported formerly and in the present study shows that the dyskinesia tends to occur in aged diabetic patients. The age of patients with dyskinesia secondary to cerebral infarction is generelly much lower. We also found that 86% (30 out of 35 cases) patients reported with HB-HC caused by non-ketotic hyperglycemia were Asians. The prognosis of the dyskinesia was excellent, and the radiological abnormalities are completely reversible.- - - - - - - - - - ranking = 0.2keywords = brain (Clic here for more details about this article) |
4/16. diffusion-weighted and gradient echo magnetic resonance findings of hemichorea-hemiballismus associated with diabetic hyperglycemia: a hyperviscosity syndrome?BACKGROUND: The magnetic resonance (MR) imaging findings of hemichorea-hemiballismus (HCHB) associated with hyperglycemia are characterized by hyperintensities in the striatum on T1-weighted MR images and computed tomographic scans, with a mechanism of petechial hemorrhage considered to be responsible. diffusion-weighted MR imaging (DWI) has been reported to detect early ischemic damage (cytotoxic edema) as bright areas of high signal intensity and vasogenic edema as areas of heterogeneous signal intensity. We report various DWI findings in 2 patients with hyperglycemic HCHB. OBJECTIVES: To describe the DWI and gradient echo findings and characterize the types of edema in HCHB associated with hyperglycemia. SETTING: A tertiary referral center neurology department. DESIGN AND methods: Two patients with HCHB associated with hyperglycemia underwent DWI, gradient echo imaging, and conventional MR imaging with gadolinium enhancement. The patients had an elevated serum glucose level on admission and a long history of uncontrolled diabetes, and the symptoms were controlled by dopamine receptor blocking agents. Initial DWIs were obtained 5 to 20 days after symptom onset. Apparent diffusion coefficient (ADC) values were measured in the abnormal lesions with visual inspection of DWI and T2-weighted echo planar images. RESULTS: T1- and T2-weighted MR images and brain computed tomographic scans showed high signal intensities in the right head of the caudate nucleus and the putamen. Gradient echo images were normal. The DWIs showed bright high signal intensity in the corresponding lesions (patient 1), and the ADC values were decreased. The decrease in ADC and the high signal intensity on DWI persisted despite the disappearance of HCHB, even after 70 days. CONCLUSIONS: Gradient echo MR imaging findings were normal in HCHB with hyperglycemia, whereas DWI and the ADC map showed restricted diffusion, which suggests that hyperviscosity, not petechial hemorrhage, with cytotoxic edema can cause the observed MR abnormalities.- - - - - - - - - - ranking = 0.2keywords = brain (Clic here for more details about this article) |
5/16. Continuous insulin infusion: promoting growth in low birth weight infants.Development of improved technologies in neonatal care has yielded increasing numbers of surviving low birth weight (LBW) infants who have challenged methods of supportive care. As researchers and practitioners have focused on respiratory, cardiac, and other body system requirements, nutritional support has been low on the priority list. Support for growth and maximized neurologic development, rather than simply for survival, has been the challenge in care of small and sick newborns. Use of insulin to enhance glucose tolerance in LBW infants, and thereby maximize growth, is a management modality that can be initiated early in the infant's course and is facilitated by implementation of clear and consistent policies and procedures. Continuous insulin infusions have been demonstrated to enhance glucose uptake and utilization--facilitating neonatal growth and in turn enhancing brain growth and developmental outcome.- - - - - - - - - - ranking = 0.2keywords = brain (Clic here for more details about this article) |
6/16. Nonketotic hyperglycemic hyperosmolar coma. Report of neurosurgical cases with a review of mechanisms and treatment.Seventy-eight critically ill patients who died while on the neurosurgical service were studied retrospectively to establish the prevalence of nonketotic hyperglycemic hyperosmolar coma (NHHC). All the patients had been comatose before death, and all underwent necropsy. Criteria for the diagnosis of NHHC included moderate-to-severe hyperglycemia with glucosuria, absence of significant acetonuria, hyperosmolarity with dehydration, and neurological dysfunction. This study revealed seven cases of unequivocal NHHC (9%), and six of hyperosmolarity but with incomplete records. Five of the seven confirmed cases of NHHC demonstrated no evidence of cerebral edema transtentorial herniation, or brain-stem damage, and showed central nervous system (CNS) lesions compatible with survival. Fatal complications of this syndrome, such as acute renal failure, terminal arrhythmias, and vascular accidents, both cerebral and systemic, were common in this series. The mechanism of coma in NHHC is believed related to shifts of free water from the cerebral extravascular space to the hypertonic intravascular space, with subsequent intracellular dehydration, accumulation of metabolic products of glucose, and brain shrinkage. It is uncertain whether injury to specific areas in the CNS is a predisposing factor to the development of NHHC. Factors documented to be significant in its development include nonspecific stress to primary illnesses, hyperosmolar tube feedings, dehydration, diabetes and mannitol, Dilantin, or steroid administration.- - - - - - - - - - ranking = 0.4keywords = brain (Clic here for more details about this article) |
7/16. Treatment of extreme hyperglycemia monitored with intracerebral microdialysis.OBJECTIVE: Description of a pediatric patient with hyperosmolar hyperglycemic nonketotic syndrome where the treatment was monitored with intracerebral microdialysis. DESIGN: Case report. SETTING: intensive care unit at a university hospital. PATIENT: An 11-yr-old boy with new-onset diabetes who presented with a blood glucose concentration of 100 mmol/L (1800 mg/dL) and a serum osmolality of 448 mOsm/kg. INTERVENTIONS: Interventions included intracerebral and subcutaneous microdialysis as well as intracranial pressure monitoring during correction of the hyperosmolar condition. The strategy was to decrease osmolality by 1 mOsm.kg(-1).hr(-1) and blood glucose by 1.5 mmol.L(-1).hr(-1) (27 mg/dL). MEASUREMENTS AND MAIN RESULTS: The concentrations of glucose in the subcutaneous dialysates corresponded to the blood glucose concentrations. The brain/subcutaneous glucose ratio varied between 0.20 and 1.28 (mean, 0.43; median, 0.4). When the blood glucose decreased quickly after steady state, the brain/subcutaneous ratio increased sharply, demonstrating that the normalization of glucose in the brain was slower than that in blood. CONCLUSIONS: microdialysis can be used to monitor the brain/subcutaneous glucose ratio in patients with extreme hyperglycemia. A rapid decrease in blood glucose increases the brain/subcutaneous glucose ratio, which may be a potential risk factor for osmotic brain edema. microdialysis may prove to be a valuable tool in treatment management. The child made a full recovery.- - - - - - - - - - ranking = 1.2keywords = brain (Clic here for more details about this article) |
8/16. Non-ketotic hyperglycaemia presenting as epilepsia partialis continua.epilepsia partialis continua (EPC) is a rare epileptic syndrome, observed in various cortical lesions and also in metabolic disorders. We report the case of a 57-year-old patient with EPC as the first manifestation of hyperosmolar non-ketotic hyperglycaemia (NKH) of diabetes mellitus. Computed tomography (CT) and magnetic resonance imaging (MRI) were normal. Initial laboratory data revealing serum glucose 1540 mg/dl, and serum osmolality 391 mOsm/l confirmed the diagnosis. electroencephalography (EEG) showed ictal discharges in the ipsilateral hemisphere during focal seizures. seizures are resistant to anticonvulsant treatment and respond best to insulin and rehydration. Focal motor seizures or EPC are commonly a symptom of NKH in the elderly patients. We recommend that in such cases a metabolic disorder such as diabetes mellitus be ruled out.- - - - - - - - - - ranking = 279.79139042133keywords = metabolic disorder (Clic here for more details about this article) |
9/16. Lactic acidosis, ketoacidosis, and energy turnover: "figure" you made the correct diagnosis only when you have "counted" on it--quantitative analysis based on principles of metabolism.Three cases are presented to illustrate that quantitative analysis based on physiologic principles can help resolve certain controversies in clinical medicine. For example, in case 1, a patient with severe hypoxia, the rate of production of lactic acid is so high that only restoration of delivery of oxygen is rational therapy. If the degree of hypoxia exceeds 5.6% of demand, dichloroacetate will not lessen the degree of acidosis. Further, even when delivery of oxygen is returned to normal, the rate of fall in lactate and rise in bicarbonate in plasma will be relatively slow. In case 2, a patient with diabetic ketoacidosis, our discussion stresses that the rate of production of ketoacids is not that rapid and that the degree of ketoacidosis is influenced to a major degree by decreasing the rate of oxidation of ketoacids in brain and kidneys. Case 3, a patient with severe hyperglycemia, illustrates that insulin will only promote the oxidation of glucose at a rapid rate once the levels of fatty acids and ketoacids decline to low levels. Accelerated transport of glucose by insulin is only a permissive action for the oxidation of glucose.- - - - - - - - - - ranking = 0.2keywords = brain (Clic here for more details about this article) |
10/16. movement disorders as a manifestation of nonketotic hyperglycemia.movement disorders are well-known presenting signs of metabolic disorders. Focal motor abnormalities may be the chief initial presentation of diabetes mellitus in the nonketotic hyperglycemic state in 6% of patients. Nonketotic hyperglycemia (NKH), in particular, may manifest any of a wide variety of movement disorders. These have been described as focal seizures, epilepsia partialis continua, myoclonus, and opsoclonia. There are descriptions of movement disorders in hyperglycemia that are similar to the coarse flapping tremor of asterixis, the posturing of paroxysmal kinetogenic choreoathetosis, and of "fencing (stance) seizures." Disorders of facial motor function including aphasia, facial muscle twitching and jerking, and disorders of muscular tone have been described. These may include hemiparesis and hemiplegias as well as increased tone, in some cases mimicking the nuchal rigidity of meningitis. The movement disorders in NKH may mimic cerebral vascular accidents, meningitis, or psychiatric disorders, as well as various types of seizures. Clinicians may be able to avoid expensive and time-consuming diagnostic evaluations to rule out NKH in patients with movement disorders. We present two patients with focal motor abnormalities associated with nonketonic hyperglycemia and review the pertinent literature.- - - - - - - - - - ranking = 139.89569521066keywords = metabolic disorder (Clic here for more details about this article) |
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