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Patient: Female, 66 Final Diagnosis: Chorea • hyperglycemia • Basal Ganglia Syndrome (C-H-BG) Symptoms: Hemibalism • hemichorea Medication: — Clinical Procedure: — Specialty: Endocrinology and Metabolic Objective: Challenging differential diagnosis Background: Hemichorea-hemiballism (HCHB) is a spectrum of involuntary, continuous non-patterned movement involving 1 side of the body. Possible causes of HCHB include hemorrhagic or ischemic stroke, neoplasm, systemic lupus erythematosus, HHNK, Wilson’s disease, and thyrotoxicosis. This case illustrates the need to be aware of hyperglycemia as a cause of hemiballism/hemichorea, which is now referred to in the medical literature as C-H-BG (chorea, hyperglycemia, basal ganglia) syndrome. Case Report: A 66-year-old Hispanic woman presented to our care with hemiballism/hemichorea of the right arm and leg of 1 week duration. She had been admitted 3 months prior with toxic metabolic encephalopathy secondary to hyperosmolar hyperglycemic non-ketotic syndrome with a blood glucose level of 984 mg/dL. Her blood glucose level was normal but hemoglobin A1C was 12.2%. A brain MRI revealed an asymmetric T1 hyperintensity of the left putamen. This specific finding was compatible with hyperglycemia-induced hemichorea hemiballism syndrome. The hemiballism/hemichorea slowly improved over the course of the hospitalization with strict glycemic control. At the 3-month follow-up visit she had no involuntary movements of her extremities, and she had well controlled blood glucose levels and a hemoglobin A1C of 9.0. Conclusions: In a patient with normal glycemic levels but a history of uncontrolled diabetes, C-H-BG syndrome should be on the top of the differential list when the characteristic MRI findings of a hyperintensity in the basal ganglia are observed. This is a rare disease that deserves attention because it is reversible with correction of hyperglycemia. Thus, prompt recognition and treatment is essential to avoid adverse outcomes.

A 63-year-old man suddenly presented with right hemiplegia and was taken to our hospital. Computed tomography (CT) scan revealed subcortical hemorrhage of the left parietal lobe. He had no medical history except hypertension; thus, it initially appeared to be a typical hypertensive hemorrhage. However, blood analysis showed an abnormally elevated activated partial thromboplastin time. One hour after admission, his Glasgow Coma Scale fell from 14 to 11. We performed an echo-guided stereotaxic removal of the hematoma. He improved immediately and was diagnosed with congenital factor XI (FXI) deficiency a few days after surgery. FXI deficiency, described as hemophilic syndrome C, rarely manifests as spontaneous bleeding, but surgical intervention has been known to manifest as bleeding. This case highlights the importance of evaluation of coagulopathies in patients with intracerebral hemorrhage before surgery, and, in cases wherein blood analysis results suggest coexisting coagulation disorders, less invasive surgical methods would likely lead to good outcomes.

In the classical Niederreiter cryptosystem a public key is the r/spl times/N matrix H/sub cr/=SH=S[z/sub j/x/sup i//sub j/], where S is a scrambling r/spl times/r matrix, distinct x/sub j//spl isin/GF(q)U(/spl infin/), and z/sub j//spl isin/GF(q)(0). Anyone who wants to send a secret message chooses a plaintext m, /spl omega//sub H/(m)/spl les/t=[(d-1)/2]=[r/2], and calculates the cyphertext as the syndrome c of the code with the parity check matrix H/sub cr/: c=mH/sup T//sub cr/. Upon receiving the ciphertext c, the legal user multiplies it by (S/sup T/)/sup -1/ and applies a fast decoding algorithm to obtain the plaintext m.

Verruculogen (V) and penitrem A (PA) represent a group of toxic secondary metabolites of mold contaminants of foodstuffs known as 'tremorgenic mycotoxins', which produce a unique neurotoxic syndrome characterized by sustained tremors, limb weakness, ataxia and convulsions. In the present study the intraperitoneal median tremogenic dose in mice for V was found to be 0.92 mg/kg and that for PA, 0.19 mg/kg. Behavioral and neurochemical parameters were assessed following acute exposure to varying neurotoxic and subneurotoxic doses of these mycotoxins. Measures of spontaneous motor activity (photoactometer) and exploratory reflex behaviors (open field) were markedly depressed by both V and PA. Notably, at dose levels of V or PA that were not accompanied by any overt signs of neurotoxicity, significant neuromotor depression was still observed. Acquisition of a conditioned avoidance shuttle response was disrupted, but only at a high neurotoxic dose level of V. Neurochemical analyses revealed no clear catecholaminergic or cholinergic involvement in the neurotoxic syndrome of eigher V or PA.