Delayed Cranial Nerve Palsy after Microvascular Decompression for Hemifacial Spasm

OBJECTIVE: Microvascular decompression (MVD) for hemifacial spasm (HFS) is a safe and effective treatment with favorable outcomes. The purpose of this study was to evaluate the incidence of delayed cranirve ( VI, VII, and VIII ) palsy following MVD and its clinical courses. METHODS: Between January 1998 and December 2009, 1354 patients underwent MVD for HFS at our institution. Of them, 100 patients (7.4%) experienced delayed facial palsy (DFP), one developed sixth nerve palsy, and one patient had delayed hearing loss. RESULTS: DFP occurred between postoperative day number 2 and 23 (average 11 days). Ninety-two patients (92%) completely recovered; however, House-Brackmann grade II facial weakness remained in eight other patients (8%). The time to recovery averaged 64 days (range, 16 days to 9 months). Delayed isolated sixth nerve palsy recovered spontaneously without any medical or surgical treatment after 8 weeks, while delayed hearing loss did not improve. CONCLUSION: Delayed cranial nerve (VI, VII, and VIII) palsies can occur following uncomplicated MVD for HFS. DFP is not an unusual complication after MVD, and prognosis is fairly good. Delayed sixth nerve palsy and delayed hearing loss are extremely rare complications after MVD for HFS. We should consider the possibility of development of these complications during the follow up for MVD.

A Case of Pulmonary Metastasis of a Dermatofibrosarcoma Protuberans / 결핵및호흡기질환

Dermatofibrosarcoma protuberans (DFPS) is a locally aggressive skin tumor with a very low incidence in the general population. This tumor has a remarkable tendency to recur, However, a metastasis is rare. We report a case of DFPS with a pulmonary metastasis in 28-year-old man. The pulmonary metastasis developed 5 years after a complete resection of the primary skin tumor. We reviewed the clinical manifestations and treatment of DFPS, and highlight the need for a long-term follow-up examination for metastases after a wide excision of these lesions.

Delayed Facial Nerve Paralysis after Middle Ear and Mastoid Surgery / 대한이비인후과학회지

BACKGROUND AND OBJECTIVES: The purpose of this study was to provide possible causes and post-treatment prognosis of delayed facial nerve palsy (DFP) following middle ear and mastoid surgery. SUBJECTS AND METHOD: The medical records of 3787 cases of middle ear and mastoid surgery from June, 1980 to August, 2003 were retrospectively reviewed. Nine cases developed ipsilateral facial nerve palsy after 72 hours of surgery. Their age ranged from 20 to 67 years (the mean of 40 years old and the male: female ratio of 1:1.25). For the review of the chart, we checked preoperative middle ear and mastoid state, intraoperative findings, clinical features of development and recovery of facial nerve palsy. To evaluate the degree and the possibility of recovery of facial nerve palsy, the House-Blackman grading system was used and electrophysiologic studies (Maximal stimulation test, Nerve excitability test and Nerve conduction velocity test) were performed. The steroid and vasodilator drugs were prescribed for the treatment. RESULTS: All of the nine patients had preoperative diagnosis of chronic otitis media and five of them also had cholesteatoma. Radical mastoidectomy was done in two cases, open cavity techniques in two cases and closed cavity techniques in five cases. There were postoperative wound infections in five cases. Facial palsy was developed between 5th and 16th postoperative day (mean 9th day) and the initial House-Blackman grade was II or III. The time for complete recovery ranged from 1 month to 6 months, with the fastest recovery time being 9 days after DFP. CONCLUSION: DFP following middle ear and mastoid surgery is an unpredictable complication. Postoperative wound infection may have been related to it and should be regarded as a risk factor of DFP.

Efecto del diisopropilfluorofosfato sobre el recambio de la serotonina en varias regiones cerebrales / Effect of the one diisopropyl fluorophosphate on the replacement of the serotonin in sereval cerebral regions

Los hallazgos de varios estudios sugieren que la interacción de la acetilcolina (ACh) y la 5-hidroxitriptamina (5-HT) participa en la regulación de procesos fisiológicos y conductuales tales como la secreción del factor liberador de corticotropina y la memorización. En el presente trabajo se estudió el efecto del diisopropilfluorosfosfato (DFP), un inhibidor irreversible de la aceticolinesterasa, sobre los niveles de 5-HT y del ácido 5-Hidroxiindolacético (5-HIAA) en seis regiones cerebrales de rata adulta. Las concentraciones de la monoamina y de su metabolito fueron medidas por cromatografía líquida de alta eficiencia (HPLC). El DFP disminuyó los niveles de 5-HIAA en el hipotálamo, sin modificación de los niveles de 5-HT. En el resto de las regiones, no se encontró modificación de los niveles de 5-HT ni de HIAA

Organophosphate Cholinesterase Inhibitor (Diisopropylfluorophosphate) Induces Acetylcholinesterase-mediated Nicotinic Receptor Facilitation

BACKGROUND: Cholinesterase inhibitors (ChEIs) which have been widely used clinically are known to have diverse actions on the neuromuscular synaptic transmissions, suggesting that inhibiting cholinesterase (ChE) might not be their only mode of action. ChEIs interact with the nicotinic acetylcholine receptor (nAChR) macromolecule as a weak agonist, and as a modulator inducing desensitization and blockade at high concentrations. In a previous study, we reported that carbamate ChEIs, Pyridostigmine and Physostigmine could facilitate the ionic influx through nAChRs, when precluding the Ach-hydrolyzing effect of acetylChE (AChE) by applying carbachol as an agonist. The facilitation of the nAChR function was supposed to be achieved by AChE-mediated nAChR modulation and possibly by the up-regulation of nAChRs. METHODS: In this study, we analyzed the effect of irreversible organophosphate ChEI, diisopropylfluorophosphate (DFP) on the function of muscular nAChRs in TE671 cells, quantifying carbachol-induced intracellular 22 Na+ influx through nAChRs, using radioassay. RESULTS: Preincubation of cells with 1 mM DFP at 37 degrees C for 10 min as well as the simultaneous application of carbachol and DFP, decreased the carbachol-induced influx dose-dependently.However, preincubation of cells with 10 micrometer DFP potentiated the influx to 132.5+/-7.4% CPM. Moreover, Najar Tx completely inhibited the potentiated 22 Na + influx. CONCLUSIONS: Organophosphate ChEI can facilitate nAChR functions at low concentrations with a yet discovered mechanism, which is supposed to necessitate cellular metabolism, and be possibly mediated by AChE. The inhibition of DFP on nAChR functions at high concentration is attributable to its remained curare-like actions and direct cellular toxicity.

Partial Purification and Characterization of 41 kDa Serine Proteinase from Culture Filtrate of Trichophyton tonsurans

Dermatophytes infect the human hair, skin, nail and cause the dermatophytosis. The extracellular and intracellular proteinases of the dermatophytes commonly occur in the genus Trichophyton like T. rubrum, T. mentagrophytes, and T. granulosum. These enzymes play a prominent role in growth, multiplication and infection of the host tissue. Extracellular proteinases have been purified from the species of Trichophyton and Microsporum. We purified the proteinase partially from the culture filtrate of the Trichophyton tonsurans through Mono-Q and Superose 12 column and investigated its biochemical and enzymatic characters. The molecular size of the proteinase was estimated to be 41 kDa by SDS-PAGE. And pI was 3.2. The optimal temperature and pH for an enzymatic activity were 27C and 7.5, respectively. The purified porteinase degraded the keratin, bovine serum albumin, hemoglobin. The serine proteinase inhibitor like PMSF and DFP inhibited the proteolytic activity of the purified enzyme whereas the cysteinase inhibitor did not. These results demonstrated that the purified proteinase is a serine proteinase and can contribute the tissue invasion.

A comparative study of delayed neurotoxicity in hens following repeated administration of organophosphorus compounds.

Hens treated with Mipafox (10 mg/kg, sc), sarin (50 micrograms/kg, sc) or parathion (1 mg/kg, sc) daily for 10 days exhibited severe, moderate and no ataxia respectively on 14th day after the start of exposure. The neurotoxic esterase (NTE) activity was significantly inhibited in the brain, spinal cord and platelets of hens treated with mipafox or sarin whereas no change was noticed with parathion treatment. All three compounds significantly inhibited acetylcholinesterase (AChE) activity in the platelets. Spinal cord of hens treated with mipafox, sarin or parathion showed axonal degeneration heavy, moderate and none respectively. It is concluded that repeated administration of equitoxic doses of mipafox, sarin and parathion to hens are marked, moderate and non-delayed neurotoxic respectively.

Assessment of Mitral Blood Flow by Exercise Doppler Echocardiography in the Diagnosis of Coronary Artery Disease

BACKGROUND: The pattern of left ventricular filling as depicted by Doppler echocardiographic transmitrial flow velocities has been used to left ventricular diastolic properties. Especially, altered transmitral flow by abnormal myocardial wall motion and left ventricular function in ischemic heart disease, was predicted during exercise test. METHODS: To determine the effects of exercise on Doppler echocardiographic measures of left ventricular diastolic filling, we studied 15 angina pectoris patients and 20 normal control subjects. Transmitral flow measurements comprised peak and integrated early passive(E) and late atrial(A) filling velocities and diastolic filling period. RESULTS: Heart rate in negative exercise treadmill test group was 70/min at rest, 111/min just after exercise, and 86/min at 5 minutes after exercise. Positive exercise treadmill test group was 69/min, 109/min and 82/min, respectively. DFP and E duration were also significantly decreased after exercise in group with negative treadmill exercise test. In positive treadmill exercise group, peak A was significantly increased from 0.57+/-0.15m/sec to 0.75+/-0.20m/sec at just after exercise(p<0.01), 0.67+/-0.12m/sec at 5 minuties after exercise. DFP and E duration were also significantly decreased after exercise. CONCLUSION: Doppler echocardiographic transmitral flow was altered by abnormal regional wall motion and left ventricular dysfunction in ischemic heart disease during exercise test. The use of Doppler echocardiography for this purpose is limited, however, because a number of variables may influence transmitral flow patterns, including age, preload, afterload and systolic function.

Isolation of a tripeptide showing weak acetylthiocholine hydrolysing activity from a soluble form of monkey basal ganglia acetylcholinesterase by limited trypsin digestion.

Acetylcholinesterase was purified from the soluble supernatant of monkey (Macaca radiata) brain basal ganglia by a three-step affinity purification procedure. The purified enzyme showed two major protein bands corresponding to molecular weights of approximately 65 kDa and approximately 58 kDa which could be labelled by [3H]diisopropylfluorophosphate. When the purified enzyme was subjected to limited trypsin digestion followed by gel filtration on Sephadex G-75 or Sephadex G-25 column, a peptide fragment of molecular weight approximately 300 Da having a weak acetylthiocholine hydrolysing activity was isolated. The amino acid sequence analysis of this peptide showed a sequence of Gly-Pro-Ser. When the [3H]DFP labelled enzyme was subjected to limited trypsin digestion and Sephadex G-75 column chromatography, a labelled peptide corresponding to approximately 430 Da was isolated. The kinetics, inhibition characteristics and binding characteristics to lectins of this peptide were compared with the parent enzyme. A synthetic peptide of sequence Gly-Pro-Ser was also found to exhibit acetylthiocholine hydrolysing activity. The kinetics and inhibition characteristics of the synthetic peptide were similar to those of the peptide derived from the purified acetylcholinesterase, except that the synthetic peptide was more specific towards acetylthiocholine than butyrylthiocholine. The specific activity (units/mg) of the synthetic peptide was about 123700 times less than that of the purified AChE.

DFP induced changes in acetylcholinesterase activity and glycogen level in certain brain regions of mice.

DFP in acute dose (2 mg/kg i. p.) in mice significantly inhibited acetylcholinesterase AChE) activity in five regions of brain i.e. cerebral cortex, corpus striatum, medulla, cerebellum and hypothalamus. The inhibition was accompanied by depletion of glycogen from these regions 1 hr after DFP administration. The inhibition of enzyme activity was more in corpus striatum and medulla and glycogen depletion was more in cerebral cortex in comparison to other regions of the brain. These changes may be due to stimulatory effect of DFP on these regions of brain in mice.

Role of liver and brain lysosomal and mitochondrial enzymes in development of delayed neuropathy in hens by 0,0-diisopropyl phosphorofluoridate.

Subacute dose of 0,0-diisopropyl phosphorofluoridate (DFP), a potent organophosphorus ester capable of producing delayed neurotoxicity (OPIDN), did not produce any significant change in the levels of lysosomal and mitochondrial marker enzymes of brain, liver and serum at any time after treatment in hens protected with atropine. The results suggest the absence of any involvement of mitochondrial and lysosomal enzymes at any stage in the development of OPIDN in susceptible species by treating with DFP.

Immunopharmacological studies on Picrorhiza kurroa Royle ex Benth. Part VI: Effect on anaphylactic activation events in rat peritoneal mast cells.

Mechanism of inhibition of mast cell anaphylaxis by P. kurroa-extract (PK) treatment in rats was investigated. Mast cell-IgE binding, assessed from induction of passive sensitization, was not affected. Calcium-independent early activation events in mast cell anaphylaxis indicated on inhibitory influence of PK-treatment. Inhibition of membrane-protease release by PK-treatment was suggested by study of gastric secretion and exhibition of saturable synergism with Di-isopropyl fluoro phosphate on inhibition of anaphylactic degranulation. pH-independence of mast cell stabilizing effect negates any PK-influence on phospholipid transmethylation. The results complement findings of earlier studies on indirect effects of PK through alteration of membrane structure/function.