Hemichorea-Hemiballismus as the First Sign of Type 1b Diabetes During Adolescence and Its Recurrence in the Setting of Infection.

Chorea may be secondary to hyperosmolar nonketotic hyperglycemia, but such situation has rarely been described in adolescents, particularly as the initial and single manifestation of type 1 diabetes. We describe a case of a previously healthy 14-year-old girl with sudden onset of choreic movements on her left upper and lower limbs. Brain computed tomography (CT) and magnetic resonance imaging (MRI) revealed an area of hyperdensity/hyperintensity affecting the right striatum. Blood glucose was 349 mg/dL. Despite adequate glucose control, the involuntary movements persisted and haloperidol, later substituted with valproate, was prescribed, with satisfactory but not complete resolution of the chorea. In 2 other occasions, when the patient had an infection and subsequent hyperglycemia, the chorea relapsed. Although not common, hyperglycemia must be considered in the differential diagnosis of acute hemichorea-hemiballismus in children and adolescents, particularly because it is a potentially reversible cause.

[Some aspects of focal infections of the head and neck region]. / Einige Gesichtspunkte zum Fokusgeschehen im Hals-Nasen-Ohren-Bereich.

The so-called focal infections are today considered to be poly-etiologic manifestations, in which there is a summation of various aggressions. The concept of focal infection is still not exactly defined. Bacterial products, toxic or antigenic substances originating from different foci are but one of the elements susceptible of unleashing the disease. This explains why there are so many foci and so few results after their elimination. The diagnosis of chronic tonsillitis or occult sinusitis especially concerning a focal disease is sometimes difficult. The ENT-specialist is responsible for both the detection of a focus in the head and neck region and its operative treatment. The interrelationship between a focal infection and its actual secondary disease must be diagnosed by the primarily inquired doctor. The diagnosis and the treatment of focal infections of the head and neck region are an interdisciplinary problem.

[Adaptation to physical and psychoemotional loads and mental work capacity in patients with neurocirculatory dystonia]. / Adaptatsiia k fizicheskim i psikhoémotsional'nym nagruzkam i umstvennaia rabotosposobnost' u bol'nykh neirotsirkuliatornoi distoniei.

Mental performance and adaptation to exercise and psychoemotional loads were studied in 119 patients with neurocirculatory asthenia (NCA), 245 patients with chronic focal infection (CFI) of the upper airways, and 247 NCA patients with CFI. Exercise tolerance was measured at spiroergometry, intellectual and psychoemotional adaptation were assessed by shifts in attention and fatigue while working with Schulte tables under conditions of time limits and the results criticism, vegetative reactivity was tested with insulin and epinephrine, variation pulsograms recorded vegetative provision of physical, intellectual and psychoemotional activity. Abnormalities in mental performance and the above adaptation related to clinical presentation of NCA and CFI as well as to vegetative regulation were registered in NCA+CFI patients. Mechanisms of the alterations observed and the role of CFI in their genesis are discussed.

[Neurocirculatory dystonia in patients with a chronic focal infection: the mechanisms of its formation and development]. / Neirotsirkuliatornaia distoniia u bol'nykh khronicheskoi ochagovoi infektsiei: mekhanizmy formirovaniia i razvitiia.

Clinical manifestations of neurocirculatory asthenia (NA) were analyzed in 604 patients with associated chronic focal infection. It is shown that the latter infection produces negative effects on clinical symptoms of NA, its course, temporary disability and effectiveness of treatment. Vegetative reactivity and vegetative activity in NA patients with the infection were affected to a greater degree than in NA patients without the focal infection. The role of afferent impulses from the nasopharynx reflexogenic zone in the genesis of clinical specificity and vegetative regulation defects in NA patients is discussed.

[The assessment of liver function in local suppurative processes (experimental research)]. / Otsenka funktsional'nogo sostoianiia pecheni pri lokal'nykh gnoinykh protsessakh (éksperimental'noe issledovanie).

The function of the liver was studied on an experimental model of a local purulent process in 40 rabbits. It is shown that a local purulent process may cause a hepatic damaging effect, the presence of which is confirmed by the active egress of the organ-specific enzymes histidase and urocaninase into the blood. Determination of these enzymes in blood serum is an authentic test which characterizes damage to the hepatic cells in a local purulent process. Appraisal of the functional condition of the liver in local purulent processes may be employed in clinical practice for early detection and timely treatment of possible hepatotoxic damage.

[Mast cells in the focus of an acute infectious inflammation]. / Tuchni klityny u vohnyshchi hostroho infektsiinoho zapaleniia.

On the model of E. coli-induced acute infectious peritonitis in rats it is established that the mast cell reaction and histamine level increase in exudate and inflamed mesentery tissue are biphase and are observed predominantly following the inflammatory agent action, in the period corresponding to the immediate phase of peritoneal cavity vessel permeability increases. The preliminary elimination of mast cells significantly inhibits a rise in the vascular permeability in the immediate phase and slightly affects the delayed phase, thus prolonging exudation. At the same time the dynamics of free histamine indicates its direct involvement in mediation and/or modulation as well as in subsequent inflammatory events. The common rules of mast cell involvement and vascular permeability increase in infectious and aseptic inflammation have been shown.

[The role of the leukocytes in increasing the vascular permeability in an infectious inflammation focus]. / Rol' leikotsytiv u pidvyshchenni pronyknosti sudyn vohnyshcha infektsiinoho zapaleniia.

The model of acute infectious peritonitis in rats with vinblastine-induced leukopenia has been used to show that the leukocyte depletion significantly influences the vascular permeability of abdominal cavity during the whole period of exudation. It inhibits the vascular permeability rise both in the immediate phase and in the initial period of delayed phase (5 h). 12 hours-5 days after the inflammatory agent action the vascular permeability under conditions of primary leukopenia appears to be more than in the natural course of inflammation, that coincides with excess of the leukocyte number usual for the inflammatory focus and with its significant increase in blood. The results indicate the essential role of leukocytes both during the immediate and delayed phases of increase in the vascular permeability of inflammatory infectious focus.

The effect of neonatal treatment with capsaicin on focal arteriolar insudation.

There is evidence that peptide neurotransmitters (e.g., substance P, neurokinin A, vasoactive intestinal peptide, calcitonin gene-related peptide) from sensory nerves play a part in vasoregulation. We examined the effect of neonatal treatment with capsaicin, a procedure that causes permanent impairment of primary sensory neurons, on a recently described arteriolar response to inflammation, focal arteriolar insudation (FAI). FAI occurs at a distance from the site of injury, in arterioles supplying that area, and is first observed 6 hr after onset of inflammation and maximally at 24 hr; the affected arterioles show dilation, with increased endothelial permeability and occasional smooth muscle cell damage. In our model, inflammation is induced by implanting a sterile plastic disk in the connective tissue superficial to the rat cremaster muscle. When carbon black is injected intravenously 24 hr later, FAI in the cremaster arterioles can be detected on light microscopy as areas of carbon extravasation; and the length of affected segments is morphometrically measured. The capsaicin-pretreated group showed a marked decrease in FAI compared to the controls. Mean FAI in the capsaicin group (12 animals) was 1.8 +/- 2.4 (SD) mm/cremaster compared to 5.6 +/- 5.1 for the control group (12 animals). P less than 0.003. These results provide evidence that this arteriolar response to inflammation is modulated in part by capsaicin-sensitive neurons.

Participation of autonomic nerve in tonsillar focal infection.

Participation of the autonomic nerve in tonsillar focal infection was investigated by measuring neurotransmitters, receptors and microvibration. In focal infection patients, the volume of norepinephrine in the tonsil increased significantly and the number of a-adrenergic receptors decreased. These findings suggest that the focally infected tonsil exhibits a high degree of sympathetic nerve activity. The ratio of N-type in microvibration decreased systematically, which indicates some imbalance or immaturity of the autonomic nervous system in focal infection patients. Based on this data, the production mechanism of tonsillar focal infection was speculated from the point of view of the autonomic nerve.

Infectious foci in chronic osteomyelitis of the jaws.

Chronic osteomyelitis of the jaws has a varied clinical appearance and an unclear etiology. In a retrospective study based on case histories and histological material from 24 patients with chronic osteomyelitis, no specific correlation could be found between clinical symptoms and morphological changes in bone. In 10 patients, bacteria were found in certain foci such as osteocytic lacunae of necrotic bone and dentinal tubules of embedded tooth fragments. In these foci, the bacteria probably escaped the immunological response as well as the antibiotic treatment. From these foci, the bacteria might maintain an inflammatory reaction in the surrounding bone. In some patients, the mandibular canal seemed to be a pathway for the spreading of the inflammatory process.