Writing behavior is affected by many factors and depends on the functional integrity of the nervous system. Its neuropsychological mechanism remains unknown. The agraphic features involving different parts of brain damage are dissimilar. The neuroanatomic location of agraphia and its possible brain mechanism are reviewed.

BACKGROUND: It is of great importance to study the genotype distribution of hereditary ataxia in understanding its epidemiologic rule and pathogenetic pathway.OBJECTIVE: To analyze the distribution of different genotype of hereditary ataxia in south China.DESIGN: A case-control observation.SETTING: Department of Neurology, the First Affiliated Hospital of Sun Yat-sen University.PARTICIPANTS: Forty-three patients (26 males and 17 females) with hereditary ataxia from 36 families and 38 patients with sporadic hereditary ataxia (24 males and 14 females) were selected from the Outpatient Clinic of Neurogenetics, Department of Neurology, the First Affiliated Hospital of Sun Yat-sen University between September 1998 and September 2002. At the same time, 60 healthy individuals from the patients' families and 44randomly-selected healthy physical examinees were taken as controls. All the participants were enrolled voluntarily.METHODS: The fragments of trinucleotide repeats at different sites of mutant genes were amplified with polymerase chain reaction (PCR), and then the lengths were calculated with polyacrylamide gel electrophoresis and imaging analytical software. The repeated numbers of trinucleotide repeats in all the normal and abnormal amplified alleles were calculated respectively.MAIN OUTCOME MEASURES: Different genotype distribution in patients with hereditary ataxia.RESULTS: All the subjects were involved in the analysis of results. Of the detected patients with hereditary ataxia, the Machado-Joseph disease/spinocerebellar ataxia (SCA) 3 was the most common type of autosomal dominant SCA in South China, which was 42.0%, and was followed by SCA2 (7.4%), SCA1 (4.9%), SCA7 (3.7%), SCA6 (2.5%), SCA12 (1.2%).No patient was detected to have SCA8 SCA 10, SCA 17 dentatorubropallidoluysian atrophy (DRPLA) and Friedreich ataxia (FRDA).CONCLUSION: Autosomal dominant SCA3 is the most familiar genotype in South China. Clinical detection of hereditary ataxia should be done firstly aiming at the SCA3 genotype.

Objective To study the molecular genetic diagnosis and clinical characteristics of spinocerebellar ataxia type 6 (SCA6).Methods 43 patients with autosomal dominant SCA from 36 families and 38 sporadic SCA patients were enrolled in the study. SCA6 (CAG)n dynamic mutations were detected by polymerase chain reaction (PCR). Abnormal allele fragments were sequenced and repeated numbers were calculated. The clinical data of two cases with SCA6 were analyzed.Results CAG repeat of normal SCA6 allele ranged from 10 to 13. CAG repeat of abnormal SCA6 allele expanded to 25 in one familial patient and 24 in one sporadic patient in our study. The basic characteristics of these SCA6 patients were slowly progressive cerebellar ataxia, nystagmus and dysarthria.Conclusion Diagnosis of SCA6 can be confirmed by detection of abnormal CAG repeat expansion. There is no obvious difference of clinical features between SCA6 and other SCA subtypes.

Objective To explore the clinical features of paroxysmal autonomic nerve dysfunction after brain injury.Methods The clinical data of 22 patients with paroxysmal autonomic never dysfunction after brain injury were analysed retrospectively.Results The 22 patients were in vegetative state.The primary injury in 14 cases were severe traumatic brain injury,2 cases were cerebral or cerebellar hemorrhage and received evacution of hematoma,1 case was heroin toxic encephalopathy,2 cases were severe carbon monoxide poisoning,3 cases were hypoxic-ischemic encephalopathy after cardiopulmonary resuscitation(1 case with electrical injury,1case with coronary angiography and coronary stent implantation and 1 case with cardiac arrest due to anaesthetic accident).They had most of the symptoms such as paroxysmal agitation,hyperthemia,diaphoresis,tachypnea,tachycardia,hypertension,myodystonia and convulsion.No epileptic wave was found on EEG in the stage of attact.Latent period of physiological waves were prolonged and amplitudes were fallen down on brain auditory evoked potential(BAEP) and somatosensory evoked potential(SEP).The lesions in varied degrees were found in the cortex,subcortex,or brainstem by neuroimaging.The medicion such as dopamine agonist or antagonist,benzodiazepines and muscle relaxants were just focused on symptoms.There were 10 cases who got out of vegetative state eventually during 1 to 13 months after onset.Conclusions The clinical features of paroxysmal autonomic nerve dysfunction after brain injury are paroxysmal autonomic nerve dysfunction combining myodystony.The most of the severe patients are in vegetative state.The therapy is only focused on symptoms.

BACKGROUND: It is commonly believed that hyperbaric oxygen (HBO)plays a neuroprotective role in the prevention and treatment of cerebral infarction (CI), however hyperbaric oxygen therapy (HBOT)-induced CI was also reported.OBJECTIVE: To investigate the risk factors of HBOT-induced CI.DESIGN: Case analysis with patients as subjects.SETTING: At the Department of Hyperbaric Oxygen of Guangzhou General Hospital of Guangzhou Military Command Area of Chinese PLA.PARTICIPANTS: Totally 192 inpatients receiving HBOT were selected from the Department of Hyperbaric Oxygen of Guangzhou General Hospital Guangzhou Military Command Area of Chinese PLA between December 1996 and March 1998, including 127 males and 65 females with age ranging from 9 to 78 years old. Totally 6 patients, 3 males and 3 females, suffered from CI during HBOT, with the age from 51 to 76 yeas.METHODS: The background factors of 192 patients who HBOT METHODS and 6 cases with induced CI were analyzed.MAIN OUTCOME MEASURES: Symptoms, signs and skull CT or MRI.RESULTS: Data of 192 patients were dealt with intentionally and all were statistically analyzed without miss. ① The incidence of CI during HBOT was 0.3% (6/192). ② The risk factors of HBOT-induced CI included: age of ≥ 60 years, hypertension, hyperlipidemia, primary CI or cerebral hemorrhage, blood hyperviscosity and diabetes, and the incidence would greatly increased in those who has 4 or more than 4 risk factors, but seldom with less than 4 risk factors.CONCLUSION: The cluster level of risk factors was closely related with the incidence of HBOT-induced CI.

BACKGROUND: Hyperbaric oxygen therapy has been considered as an effective therapy for prevention and cure of cerebral infarction traditionally.However, some scholars suggested that hyperbaric oxygen therapy could also result in cerebral infarction, although the mechanism is unclear.OBJECTIVE: To investigate the cause of cerebral infarction due to hyperbaric oxygen therapy.DESIGN: Case-control trial with patients as subjects.SETTING: Department of Hyperbaric Oxygen, Guangzhou General Hospital of Guangzhou Military Area Command of Chinese PLA.PARTICIPANTS: From December 1996 to March 1998, 192 inpatients receiving hyperbaric oxygen therapy were recruited into the trial from the Department of Hyperbaric Oxygen, Guangzhou General Hospital of Guangzhou Military Area Command of Chinese PLA. There were 127 males and 65 females aged 9-78 years. Patients admitted to the department of hyperbaric oxygen were eligible if they had hypoxia or ischemia induced disease and had no contraindication to hyperbaric oxygen therapy. Patients were recruited into the study regardless of the gender, and all patients and their family gave informed consent before enrollment. Patients were excluded if they did not receive hyperbaric oxygen therapy. According to the Diagnosis and Curing Criteria of Clinical Diseases, 6 patients developed into cerebral infarction during hyperbaric oxygen therapy, 3 males and 3 females, at the age of 51-76 years.METHODS: Patients were exposed to oxygen at 0.2 MPa in hyperbaric chamber used for many persons, and inhaled oxygen with a facemask once a day for 80 minutes with an interval of 10 minutes at the 40th minute. Ten days was considered as one course. Background and risk factors were analyzed in 6patients with cerebral infarction and 186 patients without cerebral infarction.MAIN OUTCOME MEASURES: Analysis of distribution of risk factors among cerebral infarction patients, and risk factor levels in patients without cerebral infarction.RESULTS: Among the 6 patients with cerebral infarction, hyperlipidemia was in all 6 cases, hypertension in 5 cases, primary cerebral infarction or hemorrhage in 5 cases, ≥ 60 years old or hyperviscosity in 4 cases, and diabetes mellitus in 1 case. Risk factor aggregation existed in the patients with over four risk factors. Of the 6 patients with cerebral infarction due to hyperbaric oxygen therapy, 5 cases had 4 risk factors and 1 had 5 risk factors. Of the 186 patients without cerebral infarction, 25 cases had 4 risk factors, and no case had 5 risk factors. The risk factor aggregation was relatively impossible (x2 = 54. 37, P ＜ 0. 05 ).CONCLUSION: Risk factor aggregation was found in all cerebral infarction patients, which is closely associated with the probability of cerebral infarction resulting from hyperbaric oxygen therapy.

BACKGROUND: It is believed previously that hyperbaric oxygen(HBO)therapy can prevent stroke, but some scholars think HBO therapy on the contrary can induce stroke although its pathogen and prevention are unclear.OBJECTIVE: To study the reason of cerebral thrombosis induced by HBO and the preventive effects of the medicine.DESIGN: A retrospective study based on patients as subjects.SETTING: Department of HBO in a military area command hospital ofChinese PLA.PARTICIPANTS: Totally 192 hospitalized patients receiving HBO therapy in Guangzhou General Hospital of Guangzhou Military Area Command of Chinese PLA were selected, in which there were 127 males and 65 females aged between 9 and 78 years old. A total of 6 cases including 3 male and 3 female cases aged between 51 and 76 years old developed cerebral thrombosis during therapy.METHODS: The background factors of 192 patients who received HBO therapy and the included 6 cerebral thrombosis cases were analyzed. Totally preventive effects of the medicine on a cluster level of different risk factor. Three groups of patients received different interventions under the prerequisites of routine medications including blood-activating and stasis-eliminating, neurotrophy, and vasodilator patients of nitric ether group received oral administration of isosorbide dinitrate or glycerin trinitrate; patients of calcium antagonist group received oral administration of Sibelium or Novarsc; and patients of no specific medication group did not receive any preventive medicine.MAIN OUTCOME MEASURES: Patients' symptoms, physical signs andhead CT or MRI.RESULTS: The risk factor of cerebral thrombosis induced by HBO was the basic disease of hyperlipidemia or hypertension, etc. A total of 115 cases had the cluster with less than 4 risk factors and none of them developed thrombosis. A total of 31 cases had the cluster with 4 or more than 4 risk factors and 6 of them developed thrombosis with greatly increased morbidity. Above the level of 4 risk factors, nitrate ether had effective preventive effect(0/13) while there was 33.3% of the patients(5/15) in calcium antagonist group developed thrombosis, and the difference between the above two groups was significant( P ＜ 0.05).CONCLUSION: The cluster level of risk factors has close relationship with the probability of thrombosis induced by HBO. Nitrate ether has significant preventive effects.

BACKGROUND: Hyperbaric oxygen may induce cerebral infarction. But what kind of medicine may prevent it and what is the preventive function of the medicine are not clear yet.OBJECTIVE: To compare the preventive function of nitrates with calcium antagonists in cerebral infarction induced by hyperbaric oxygen.DESIGN: Controlled retrospective observation based on patients.SETTING: Department of Hyperbaric Oxygen, Department of Neurology,Guangzhou General Hospital of Guangzhou Military Area Command of Chinese PLA.PARTICIPANTS: Totally 192 patients receiving hyperbaric oxygen treatment in Guangzhou General Hospital of Guangzhou Military Area Command of Chinese PLA, who were 127 males and 65 females, and aged 9 -78 years old. Among them, 6 patients developed into cerebral infarction.METHODS: Totally 192 patients receiving hyperbaric oxygen treatment were old, hypertensive disease, hyperlipemia, cerebral infarction(or cerebral hemorrhage), hyperviscosity in blood and diabetes as dangerous factors, prevention function of medicine was analyzed on the level of grouping different dangerous factors.INTERVENTIONS: Under the prerequisite condition of regular treatment medicine given to the 192 patients of the 3 groups, patients in nitrate group took isosorbide dinitrate or nitroglycerin orally, patients in calcium antagonist group took sibelium or Norvasc and so on orally, and patients in group without special medication did not take preventive drugs.MAIN OUTCOME MEASURES: Dangerous index was dangerous factorsto cerebral infarction.RESULTS: No one developed into cerebral infarction with grouping less than 4 dangerous factors. On the level of grouping 4 or more dangerous factors,nitrates had good preventive function, but in calcium antagonist group,33.3% patients developed into cerebral infarction. There was significant difference between them( P ＜ 0.05).CONCLUSION: Nitrates have significant preventive functions, but calcium antagonists have no such functions.

With the global warming, the incidence of heat stroke was significantly higher than before. Severe heat stroke has a high mortality, high morbidity and consolidated central nervous system injury characteristics. The main features of severe heat stroke cerebral injury include cognitive impairment, delirium, convulsions and coma. Its mechanism is related with heat shock induced cerebral tissue ischemia and hypoxia, vascular dysfunction, secondary cascade inflammation and so on. Currently, the main treatment of heat stroke cerebral injury is the hypothermia therapy, dehydration for the reduction of intracranial pressure, naloxone and other cerebral protection and nutrition treatments. Hyperbaric oxygen therapy (HBOT) is effective in treating brain injury. HBOT can alleviate tissue ischemia and hypoxia, improve circulation, reduce cerebral edema, and anti-inflammatory, anti-oxidative damage, anti-apoptosis and other molecular biological effects. HBOT also play a wake up-promoting effect of nerve repair in the cerebral injury. The treatment of cerebral injury has been the difficulty and weakness of heat stroke research. Therefore, this article reviewed the epidemiology, pathogenesis, the therapeutic effect and mechanism of hyperbaric oxygen on cerebral injury in severe heat stroke to clarify the advantages of HBOT and to provide experimental basis for further research.