Diphtheritic polyneuropathy: clinical analysis of severe forms.

BACKGROUND: Diphtheritic polyneuropathy (DP) is a dangerous complication of diphtheria, especially its severe forms with bulbar, respiratory tract, and circulatory disturbances. However, the clinical picture of severe forms of DP is practically unknown. OBJECTIVE: To investigate the clinical features and peculiarities of the course of severe forms of DP. PATIENTS: Thirty-two patients with severe forms of DP. RESULTS: The first symptoms of DP developed in most patients 3 to 5 weeks after the onset of diphtheria. The cranial nerves were involved in all patients, most frequently nerves IX and X (32 patients); VII (28 patients); III, IV, and VI (27 patients); and XI (27 patients). One third of the patients had quadriplegia. The remaining patients had quadripareses. Of the 32 patients, 24 underwent artificial ventilation. All patients had sensory signs, proprioceptive more often than superficial. Autonomic disturbances were observed also in all patients. Only 2 of the 32 patients died. CONCLUSIONS: A direct indication for tracheotomy and artificial ventilation in patients with DP is a decrease of the vital capacity of the lungs below the traditional 16 mL/kg body weight or the development of the paralytic closure of the larynx against the background of the increasing weakness of the respiratory muscles. Characteristic of severe forms of DP is the phenomenon of the oppositely directed change in the neurological symptoms in the second month of the disease: the restoration of the function of the cranial nerves against the background of the further increase of the motor disturbances in the extremities and trunk. Special attention and care should be taken of patients during the period of the appearance of the episodes of vascular collapses-between the fourth and seventh weeks of DP.

[Expression of NADPH-diaphorase in the peripheral nerve and its changes at different stages of diphtheritic polyneuropathy]. / Ekspressiia NADPH-diaforazy v perifericheskom nerve i ee izmenenie na raznykh stadiiakh difteriinoi polineiropatii.

Distribution and intensity of NADPH-d reactivity, a marker for enzyme of the nitric oxide synthesis, in nervus suralis biopsies in severe DP were studied at light and electron microscopic levels. The study of control specimens has shown that NADPH-d reactivity was permanently present in Schwann cells (SC) and was distributed in all parts of their cytoplasm. Axon and myelin were devoid of NADPH-d reactivity. A decrease of enzyme reactivity in SC cytoplasm of the damaged nerve fibers and rising enzyme reactivity in the cytoplasm of activated SC were observed in DP. High reactivity in SC of small fibers was found at earlier stages and that of thick fibers at later stages. This distinction reflected, apparently, sequence of entering at first thin, then thick fibres in the reparative process. Under the electron microscope, the reaction product was deposited on membranes of endoplasmic reticulum, nuclear membrane and Golgi complex. The enzyme was also located in nucleus of activated SC. Ultrastructural location and the fact that the highest intensity of reaction is present in SC of nervous fibres with morphological signs of remyelination suggest link of this enzyme with the reparative process. This study provides the first evidence of NADPH-d reactivity in SC and shows that NADPH-d histochemistry is a useful tool for peripheral nerve biopsies study.

[Diphtheritic polyneuropathy: clinico-morphologic study]. / Difteriinaia polineiropatiia: kliniko-morfologicheskoe issledovanie.

18 patients with grave DP treated with a long-term artificial pulmonary ventilation and feeding through a naso-gastric probe were studied. Biopsies of n. suralis taken at different periods after the appearance of the first signs of DP (from the 19th to the 69th day) were studied at light and electronic microscopy. The basis of DP is toxic myelopathy with paranodal demyelination mainly in the large myelinated neural fibers and a segmentary one in the smaller neural fibers. Axonal degeneration was observed in the gravest cases of DP and was secondary being the result of axon squeezing by a folded myelin and voluminous Schwann cell cytoplasm invaginated into the axon. In no case of DP inflammatory changes and(or) involvement of the immunocompetent cells were found. There was pronounced proliferation and activation of Schwann cells due to intensive utilization of the degradation products of myelin and remyelinization. Morphological signs of remyelinization were observed on the 35th day of DP in the presence of enhancing neurological symptoms. But remyelinization was not complete even on the 69th day of DP.

[Course of apallic syndrome after clinical death during anesthesia]. / Evoliutsiia apallicheskogo sindroma posle klinicheskoi smerti v narkoze.

Anesthesiological errors after clinical death during narcosis for strumectomy are considered. These errors were continuation of surgery after systole, inadequate management of the systemic arterial pressure and cerebral circulation after global ischemia, early switch-off of artificial ventilation of the lungs. All these steps led to prolonged coma, development of the apallic syndrome, and invalidism of the patient.

[Plasmapheresis and hormone therapy in severe forms of Guillain-Barré syndrome]. / Plazmaferez i gormonoterapiia pri tiazhelykh formakh sindroma Giiena- Barre.

Patients with severe Guillain-Barre syndrome were entered into 2 groups: group I was treated with hormones alone, group II with hormones plus plasmapheresis. The results were not significantly different. In view of recognized effectiveness of plasmapheresis for treatment of the syndrome, corticosteroid addition is inappropriate.

[Thrombolytic therapy with streptodekase in ischemic strokes]. / Tromboliticheskaia terapiia streptodekazoi pri ishemicheskom insul'te.

Thrombolytic agents previously employed in the treatment of ischemic stroke were associated with adverse side-effects and hemorrhagic complications. The use of streptodekase (S), a Soviet trombolytic drug, which is a long-acting immobilized ensyme proved to be highly effective. The efficacy of S in ischemic stroke was not investigated. The authors report the use of S within the first 6-8 hours after an ischemic stroke in thrombosis of the main stem of the middle meningeal artery in one case and of the vertebral and main arteries with the development of the locked-in syndrome in the other. In both cases the administration of S led to thrombolysis and restoration of the blood flow. The authors discuss the results of the use of S and indicate the necessity of the earliest possible administration of the drug with regard to a high sensitivity of the brain to ischemic lesions.