Prevention and treatment of pressure sore following spinal cord injury

Pressure sores or pressure injury is a serious complication of a spinal cord injury (SCI), representing a challenging problem for patients, their caregivers, and their physicians. Persons with SCI are vulnerable to pressure sores throughout their life. Pressure sores can potentially interfere with the physical, psychosocial, and overall quality of life. Outcomes directly depend on education and prevention along with conservative and surgical management. Therefore, it is very important to understand everything about pressure sores following SCI. This review covers epidemiology, cost, pathophysiology, risk factors, staging, evaluation tools, prevention, education, conservative wound care methods, surgical treatment, and future trends in wound healing related to post-SCI pressure sores. A change in nomenclature was adopted by the National Pressure Ulcer Advisory Panel in 2016, replacing “pressure ulcer”with “pressure injury.” New concepts of pressure injury staging, such as suspected deep tissue injuries and unstageable pressure injuries, were also introduced. A systematic evidence-based review of the prevention of and therapeutic interventions for pressure sores was also discussed.

Baicalin alleviates lipopolysaccharide-induced neuroglial activation and inflammatory factors activation in hippocampus of adult mice / 한국실험동물학회지

Baicalin is a natural flavonoid that exerts a variety of pharmaceutical effects such as anti-inflammatory and antioxidant. Lipopolysaccharide (LPS) is an endotoxin that releases inflammatory cytokines and induces inflammatory response. This study was investigated the anti-inflammatory mechanism of baicalin against LPS-induced inflammatory response in the hippocampus. Adult mice were randomly grouped into control, LPS-treated, and LPS and baicalin co-treated animals. LPS (250 μg/kg/day) and baicalin (10 mg/kg/day) were administered intraperitoneally for 7 consecutive days. We measured neuroglia cells activation and inflammatory factors activation using Western blot analysis and immunofluorescence staining techniques. Ionized calcium binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) are widely used as microglia and astrocyte markers, respectively. LPS treatment increased Iba-1 and GFAP expression, while baicalin co-treatment attenuated this overexpression. Nuclear factor-kappa B (NF-κB) is a key mediator of inflammation. Baicalin co-treatment alleviated LPS-induced increase of NF-κB in the hippocampus. In addition, LPS treatment upregulated pro-inflammatory cytokines including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). However, baicalin co-treatment prevented LPS-induced increases of IL-1β and TNF-α in the hippocampus. Results from the present study showed that baicalin suppresses LPS-induced neuroinflammation by regulating microglia and astrocyte activation and modulating inflammatory factors in the hippocampus. Thus, these results demonstrate that baicalin has neuroprotective effect by alleviates microglia and astrocyte activation and modulates inflammatory response by suppressing NF-κB expression in hippocampus with neuroinflammation caused by LPS.

Lipopolysaccharide induces neuroglia activation and NF-κB activation in cerebral cortex of adult mice / 한국실험동물학회지

Lipopolysaccharide (LPS) acts as an endotoxin, releases inflammatory cytokines, and promotes an inflammatory response in various tissues. This study investigated whether LPS modulates neuroglia activation and nuclear factor kappa B (NF-κB)-mediated inflammatory factors in the cerebral cortex. Adult male mice were divided into control animals and LPS-treated animals. The mice received LPS (250 µg/kg) or vehicle via an intraperitoneal injection for 5 days. We confirmed a reduction of body weight in LPS-treated animals and observed severe histopathological changes in the cerebral cortex. Moreover, we elucidated increases of reactive oxygen species and oxidative stress levels in LPS-treated animals. LPS administration led to increases of ionized calcium-binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) expression. Iba-1 and GFAP are well accepted as markers of activated microglia and astrocytes, respectively. Moreover, LPS exposure induced increases of NF-κB and pro-inflammatory factors, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Increases of these inflammatory mediators by LPS exposure indicate that LPS leads to inflammatory responses and tissue damage. These results demonstrated that LPS activates neuroglial cells and increases NF-κB-mediated inflammatory factors in the cerebral cortex. Thus, these findings suggest that LPS induces neurotoxicity by increasing oxidative stress and activating neuroglia and inflammatory factors in the cerebral cortex.

Hyperglycemia aggravates decrease in alpha-synuclein expression in a middle cerebral artery occlusion model / 한국실험동물학회지

Hyperglycemia is one of the major risk factors for stroke. Hyperglycemia can lead to a more extensive infarct volume, aggravate neuronal damage after cerebral ischemia. α-Synuclein is especially abundant in neuronal tissue, where it underlies the etiopathology of several neurodegenerative diseases. This study investigated whether hyperglycemic conditions regulate the expression of α-synuclein in middle cerebral artery occlusion (MCAO)-induced cerebral ischemic injury. Male Sprague-Dawley rats were treated with streptozotocin (40 mg/kg) via intraperitoneal injection to induce hyperglycemic conditions. MCAO were performed four weeks after streptozotocin injection to induce focal cerebral ischemia, and cerebral cortex tissues were obtained 24 hours after MCAO. We confirmed that MCAO induced neurological functional deficits and cerebral infarction, and these changes were more extensive in diabetic animals compared to non-diabetic animals. Moreover, we identified a decrease in α-synuclein after MCAO injury. Diabetic animals showed a more serious decrease in α-synuclein than non-diabetic animals. Western blot and reverse-transcription PCR analyses confirmed more extensive decreases in α-synuclein expression in MCAO-injured animals with diabetic condition than these of non-diabetic animals. It is accepted that α-synuclein modulates neuronal cell death and exerts a neuroprotective effect. Thus, the results of this study suggest that hyperglycemic conditions cause more serious brain damage in ischemic brain injuries by decreasing α-synuclein expression.

Hyperglycemia exacerbates downregulation of dynamin-like protein 1 in ischemic cerebral injury / 한국실험동물학회지

Ischemic stroke is one of the leading causes of adult disability and death. Hyperglycemia is associated with an increased risk of stroke and poor outcomes after brain injury. Dynamin-like protein I (DLP-1) regulates mitochondrial fission and promotes mitochondrial dynamics. Neurodegenerative diseases are associated with mitochondrial dysfunction, and the downregulation of DLP-1 has been previously identified in a stroke animal model. Here, we investigated the changes in DLP-1 protein expression in an animal model of focal cerebral ischemia with induced hyperglycemia. Streptozotocin (40 mg/kg) was intraperitoneally injected into male rats to induce hyperglycemia, and middle cerebral artery occlusion (MCAO) was surgically induced 4 weeks after streptozotocin treatment. Brain tissue was isolated 24 hours after MCAO, and cerebral cortex samples were used for this study. Proteomics revealed a decrease in DLP-1 expression in MCAO animals when compared with controls, and this downregulation was more prominent in MCAO animals with hyperglycemia. Reverse-transcription polymerase chain reaction and Western blot analyses confirmed that DLP-1 was significantly downregulated in MCAO-injured animals with hyperglycemia compared to those without hyperglycemia. The decrease in DLP-1 indicates mitochondrial morphological changes and dysfunction. Together, these results suggest that the severe decrease of DLP-1 seen after brain injury under hyperglycemic conditions may exacerbate the damage to the brain.

Quercetin attenuates the injury-induced reduction of γ-enolase expression in a middle cerebral artery occlusion animal model / 한국실험동물학회지

Quercetin, a natural flavonoid, copiously exists in vegetable, fruits and tea. Quercetin is beneficial to neurodegenerative disorders via its strong anti-oxidant and anti-inflammatory activities. γ-Enolase is one of the enzymes of glycolytic pathway and is predominantly expressed in neuronal cells. The aim of the present study is to verify whether quercetin modulates the expression of γ-enolase in brain ischemic injury. Adult Sprague-Dawley male rats were subjected to middle cerebral artery occlusion (MCAO) and quercetin (50 mg/kg) or vehicle was administered by intraperitoneal injection at 1 h before MCAO onset. A proteomics study, Western blot analysis, reversetranscription-PCR, and immunofluorescence staining were conducted to investigate the change of γ-enolase expression level. We identified a decline in γ-enolase expression in MCAO-operated animal model using a proteomic approach. However, quercetin treatment significantly attenuated this decline. These results were confirmed using Western blot analysis, reverse transcription-PCR, and immunofluorescence staining techniques. γ-Enolase is accepted as a neuron specific energy synthesis enzyme, and quercetin modulates γ-enolase in a MCAO animal model. Thus, our findings can suggest the possibility that quercetin regulates γ-enolase expression in response to cerebral ischemia, which likely contributes to the neuroprotective effect of quercetin.

Korean Database of Cerebral Palsy: A Report on Characteristics of Cerebral Palsy in South Korea

OBJECTIVE: To introduce the Korean Database of Cerebral Palsy (KDCP) and to provide the first report on characteristics of subjects with cerebral palsy (CP). METHODS: The KDCP is a nationwide database of subjects with CP, which includes a total of 773 subjects. Characteristics such as demography, birth history, onset and type of CP, brain magnetic resonance imaging (MRI) findings, functional ability and accompanying impairments, were extracted and analyzed. RESULTS: Preterm delivery and low birth weight were found in 59.51% and 60.28% of subjects, respectively. Postnatally acquired CP was 15.3%. The distribution of CP was 87.32%, 5.17%, and 1.81% for spastic, dyskinetic, and ataxic types, respectively. Functional ability was the worst in dyskinetic CP, as compared to other types of CP. Speech-language disorder (43.9%), ophthalmologic impairment (32.9%), and intellectual disability (30.3%) were the three most common accompanying impairments. The number of accompanying impairments was elevated in subjects with preterm birth and low birth weight. Brain MRI showed normal findings, malformations, and non-malformations in 10.62%, 9.56%, and 77.35% of subjects, respectively. Subjects with normal MRI findings had better functional ability than subjects with other MRI findings. MRI findings of a non-malformation origin, such as periventricular leukomalacia, were more common in subjects with preterm birth and low birth weight. CONCLUSION: The KDCP and its first report are introduced in this report, wherein the KDCP established agreement on terminologies of CP. This study added information on the characteristics of subjects with CP in South Korea, which can now be compared to those of other countries and ethnicities.

Effects of Exercise on Neuropathy in Streptozotocin-Induced Diabetic Rats

OBJECTIVE: To evaluate the effects of early regular exercise and to assess the electrophysiological and histopathological findings of the rat tail nerve in relation to the timing of exercise training for swimming exercise in rats with diabetic neuropathy. METHODS: We used 70 Sprague-Dawley male rats, and the experimental group comprised 60 rats, and the control group comprised 10 rats. Diabetes was induced by intraperitoneal injection of streptozotocin. Blood glucose concentrations were measured in tail vein blood samples. The experimental group was divided into 6 subgroups according to insulin treatment and swimming exercise: group 1, diabetic control; group 2, insulin treated; group 3, insulin untreated with early swimming exercise; group 4, insulin treated and early swimming exercise; group 5, insulin treated and late swimming exercise; and group 6, insulin untreated with late swimming exercise. Sensory and motor nerve conduction studies were performed weekly up to the 13th week using rat tail nerves. The effect on structural diabetic neuropathy was assessed by morphometry and ultrastructural examination of the rat tail nerve fiber at the 14th week. RESULTS: An exercise effect was observed in the insulin treated groups, but it was not observed in the insulin untreated groups. The sensory nerve conduction study in the rat tail revealed significantly prolonged latency and decreased amplitude in groups 1 and 6, and a further delay was observed in group 5 when compared to group 4. Decreased thickness of myelin was found in groups 1 and 6 through morphometry. CONCLUSION: Early regular exercise programs in addition to conventional insulin treatment may retard the progression of diabetic peripheral neuropathy.

Changes in Resting Calcaneal Stance Position Angle Following Insole Fitting in Children With Flexible Flatfoot

OBJECTIVE: To clarify the relationship of the initial radiologic and a biomechanical parameter at first clinical visit, and define the effectiveness of modified insole, following insole fitting in children with flexible flatfoot. METHODS: Children aged less than 13 years with flexible flatfoot were enrolled. The total number of subjects was 66 (33 boys, 33 girls). The subjects were divided into 5 subgroups, based on age: 1–2, 3–4, 5–6, 7–9, and 10–12 years. The mean time period between the initial & final examination for their resting calcaneal stance position angle (RCSPA) was 24 months. Radiography quantified the deformity by measuring angles, including the talometatarsal angle, the metatarsal angle, and the calcaneal pitch angle. RESULTS: From the angles measured on radiographs, only the talometatarsal angle showed a statistically significant correlation to the initial RCSPA (r=-0.578 for right side, r=-0.524 for left side; p<0.01). The mean RCSPA improved in all subgroups of subjects following insole fitting. Moreover, in children younger than 7 years, the improvement in RCSPA from the insole fitting was greater compared to children aged 7 years and older. CONCLUSION: The insole has additionally beneficial effects in all populations younger than 13 years. However, there might exist a hidden effect of normal structural pedal alignment during growth accompanied with bony maturation and developmental process. To date, it is controversial whether the treatment of flexible flatfoot is necessary in the vast majority of cases, or simple observation and advice to parents would suffice.

Metformin attenuate PTZ-induced apoptotic neurodegeneration in human cortical neuronal cells

Objective: Seizures are one of the neurodegenerative disorders of human being. Metformin has antioxidant properties and commonly used as an oral antidiabetic drug. The current study was aimed to observe the neuroprotective effect of metformin against PTZ-induced apoptotic neurodegeneration in human cortical neuronal cell culture

Methods: To observe that exposure of pentylenetetrazol [PTZ] at the dose of [30mM] for 30 minutes induced neuronal cell death by activation of caspase-3 in human cortical neuronal 2 [HCN-2] cell line. While the metformin at the dose of [20mM] along with PTZ for 30 minutes showed neuroprotection against PTZ-induced neuronal cell loss by MTT assay and Western blot analysis

Results: The results of this study showed that PTZ-induced neuronal cell death by activation of pro apoptotic proteins caspase-3 and 9 whereas the exposure of metformin showed its protective effect against neuronal loss in HCN-2 cell line. Finally, our results showed that exposure of metformin can prevent the harmful effect induced by PTZ in neuronal cells cultures

Conclusions: Our finding suggest that metformin exposure attenuates PTZ-induced neuronal cell death may act as a safe therapeutics and neuroprotective agent for the treatment of neuronal loss as result of seizure

Factors Related to the Occurrence of Urinary Tract Infection Following a Urodynamic Study in Patients With Spinal Cord Injury

OBJECTIVE: To analyze the factors related to urinary tract infection (UTI) occurrence after an urodynamic study (UDS) in patients with spinal cord injury (SCI). METHODS: We retrospectively investigated the medical records of 387 patients with SCI who underwent UDS with prophylactic antibiotic therapy between January 2012 and December 2012. Among them, 140 patients met the inclusion criteria and were divided into two groups, UTI and non-UTI. We statistically analyzed the following factors between the two groups: age, sex, level of injury, SCI duration, spinal cord independence measure, non-steroidal anti-inflammatory drug use, diabetes mellitus, the American Spinal Injury Association impairment scale (AIS), lower extremity spasticity, a history of UTI within the past 4 weeks prior to the UDS, symptoms and signs of neurogenic bladder, urination methods, symptoms during the UDS and UDS results. RESULTS: Among the 140 study participants, the UTI group comprised 12 patients and the non-UTI group comprised 128 patients. On univariate analysis, a history of UTI within the past 4 weeks prior to the UDS was significant and previous autonomic dysreflexia before the UDS showed a greater tendency to influence the UTI group. Multivariable logistic regression analysis using these two variables showed that the former variable was significantly associated with UTI and the latter variable was not significantly associated with UTI. CONCLUSION: In patients with SCI, a history of UTI within the past 4 weeks prior to the UDS was a risk factor for UTI after the UDS accompanied by prophylactic antibiotic therapy. Therefore, more careful pre-treatment should be considered when these patients undergo a UDS.

Abnormal Ocular Movement With Executive Dysfunction and Personality Change in Subject With Thalamic Infarction: A Case Report

The thalamus, located between the cerebrum and midbrain, is a nuclear complex connected to the cerebral cortex that influences motor skills, cognition, and mood. The thalamus is composed of 50-60 nuclei and can be divided into four areas according to vascular supply. In addition, it can be divided into five areas according to function. Many studies have reported on a thalamic infarction causing motor or sensory changes, but few have reported on behavioral and executive aspects of the ophthalmoplegia of the thalamus. This study reports a rare case of a paramedian thalamus infarction affecting the dorsomedial area of the thalamus, manifesting as oculomotor nerve palsy, an abnormal behavioral change, and executive dysfunction. This special case is presented with a review of the anatomical basis and function of the thalamus.

Concomitant Acute Transverse Myelitis and Sensory Motor Axonal Polyneuropathy in Two Children: Two Case Reports

Acute transverse myelitis (ATM) is an upper motor neuron disease of the spinal cord, and concomitant association of peripheral polyneuropathy, particularly the axonal type, is rarely reported in children. Our cases presented with ATM complicated with axonal type polyneuropathy. Axonal type polyneuropathy may be caused by acute motor-sensory axonal neuropathy (AMSAN) or critical illness polyneuropathy and myopathy (CIPNM). These cases emphasize the need for nerve and muscle biopsies to make the differential diagnosis between AMSAN and CIPNM in patients with ATM complicated with axonal polyneuropathy.

Changes of Functional Outcomes According to the Degree of Completeness of Spinal Cord Injury

OBJECTIVE: To evaluate whether an initial complete impairment of spinal cord injury (SCI) contributes to the functional outcome prediction, we analyzed the relationship between the degree of complete impairment according to the American Spinal Injury Association impairment scale (AIS), the posterior tibial nerve somatosensory evoked potential (PTSEP) and the changes of functional indices. METHODS: Sixty subjects with SCI were studied who received rehabilitative management for over 2 months. The degree of completeness on basis of the initial AIS and PTSEP were evaluated at the beginning of rehabilitation. Following treatment, several functional indices, such as walking index for spinal cord injury version II (WISCI II), spinal cord independence measure version III (SCIM III), Berg Balance Scale (BBS), and Modified Barthel Index (MBI), were evaluated until the index score reached a plateau value. RESULTS: The recovery efficiency of WISCI and BBS revealed a statistically significant difference between complete and incomplete impairments of initial AIS and PTSEP. The SCIM and MBI based analysis did not reveal any significant differences in terms of the degree of AIS and PTSEP completeness. CONCLUSION: AIS and PTSEP were highly effective to evaluate the prognosis in post-acute phase SCI patients. BBS and WISCI might be better parameters than other functional indices for activities of daily living to predict the recovery of the walking ability in post-acute SCI.

Arnold-Chiari Malformation Type III With Meningoencephalocele: A Case Report

Arnold-Chiari malformation type III (CM III) is an extremely rare anomaly with poor prognosis. An encephalocele with brain anomalies as seen in CM II, and herniation of posterior fossa contents like the cerebellum are found in CM III. The female infant was a twin, born at 33 weeks, weighing 1.7 kg with a huge hydrocele on the craniocervical junction. After operations were performed, she was referred to the department of rehabilitation medicine for poor motor development, swallowing dysfunction, and poor eye fixation at 22 months. The child was managed with neurodevelopmental treatment, oromotor facilitation, and light perception training. After 14 months, improvement of gross motor function was observed, including more stable head control, rolling, and improvement of visual perception. CM III has been known as a condition with poor prognosis. However, with the improvement in operative techniques and intensive rehabilitations, the prognosis is more promising than ever before. Therefore, more attention must be paid to the rehabilitation issues concerning patients with CM III.

Multiple Cranial Neuropathies Without Limb Involvements: Guillain-Barre Syndrome Variant?

Acute multiple cranial neuropathies are considered as variant of Guillain-Barre syndrome, which are immune-mediated diseases triggered by various cases. It is a rare disease which is related to infectious, inflammatory or systemic diseases. According to previous case reports, those affected can exhibit almost bilateral facial nerve palsy, then followed by bulbar dysfunctions (cranial nerves IX and X) accompanied by limb weakness and walking difficulties due to motor and/or sensory dysfunctions. Furthermore, reported cases of the acute multiple cranial neuropathies show electrophysiological abnormalities compatible with the typical Guillain-Barre syndromes (GBS). We recently experienced a patient with a benign infectious disease who subsequently developed symptoms of variant GBS. Here, we describe the case of a 48-year-old male patient who developed multiple symptoms of cranial neuropathy without limb weakness. His laboratory findings showed a positive result for anti-GQ1b IgG antibody. As compared with previously described variants of GBS, the patient exhibited widespread cranial neuropathy, which included neuropathies of cranial nerves III-XII, without limb involvement or ataxia.

Changes of Musculoskeletal Deformity in Severely Disabled Children Using the Custom Molded Fitting Chair

OBJECTIVE: To know the effectiveness of a custom molded fitting chair between pre- and post-chair status through comparison of musculoskeletal indices in severely disabled children. METHODS: We researched 34 severely disabled patients who had used a custom molded fitting chair continuously for more than a year. There were 27 cerebral palsy patients and 7 patients with other kinds of diseases that affect the brain such as chromosomal disease or metabolic disease. By radiographic studies, Cobb's angle, the femoral neck-shaft angle of the femur, and Reimers migration percentage were measured. The indices are analyzed before and after application. RESULTS: The average period of application was 24 months. There was a significant reduction in the angles of femur neck-shaft, 163.4 degree before and 158.2 degree after the use of the chair (p<0.05), and 23 of 34 had demonstrated a reduced angle. Cobb's angle and Reimers migration percentage increased but the difference of pre- and post-chair status was not statistically significant. Seventeen of 33 children showed reduced Cobb's angle. Also, 19 of 37 showed a reduced degree of dislocation of the hip joints. CONCLUSION: In spite of the use of a custom molded fitting chair, a significant improvement did not emerge for musculoskeletal deformity indices in severely disabled children. However, there was no significant aggravation of Cobb's angle or Reimers migration percentage in developing children. Therefore, it is thought be helpful to prevent rapid aggravation of musculoskeletal deformities.

Ferulic acid regulates the AKT/GSK-3beta/CRMP-2 signaling pathway in a middle cerebral artery occlusion animal model / 한국실험동물학회지

Ferulic acid, a component of the plants Angelica sinensis (Oliv.) Diels and Ligusticum chuanxiong Hort, exerts a neuroprotective effect by regulating various signaling pathways. This study showed that ferulic acid treatment prevents the injury-induced increase of collapsin response mediator protein 2 (CRMP-2) in focal cerebral ischemia. Glycogen synthase kinase-3beta (GSK-3beta) regulates CRMP-2 function through phosphorylation of CRMP-2. Moreover, the pro-apoptotic activity of GSK-3beta is inactivated by phosphorylation by Akt. This study investigated whether ferulic acid modulates the expression of CRMP-2 and its upstream targets, Akt and GSK-3beta, in focal cerebral ischemia. Male rats were treated immediately with ferulic acid (100 mg/kg, i.v.) or vehicle after middle cerebral artery occlusion (MCAO), and then cerebral cortices were collected 24 hr after MCAO. MCAO resulted in decreased levels of phospho-Akt and phospho-GSK-3beta, while ferulic acid treatment prevented the decrease in the levels of these proteins. Moreover, phospho-CRMP-2 and CRMP-2 levels increased during MCAO, whereas ferulic acid attenuated these injury-induced increases. These results demonstrate that ferulic acid regulates the Akt/GSK-3beta/CRMP-2 signaling pathway in focal cerebral ischemic injury, thereby protecting against brain injury.

Rho GTPase activating protein 15 [arhGAP15] siRNA effect apoptosis-induced by ethanol in bovine fibroblast cells

The Rho GTPases are the sub-group of Ras super family and identified in all eukaryotes. The Rho GTPases effect different cellular signaling pathways involved in a number of diseases such as cancer, neurological and cardiovascular disorders. Members of Rho GTPases including RhoA, RhoC and Rac1 play a major role in regulation of apoptosis in different kind of stress conditions. Here we investigated the Rho GTPase activating protein 15 [ArhGAP15] gene knock-down effect on apoptosis induced by ethanol in bovine fibroblast cells. The bovine Fibroblast cells were treated and transfected with two different concentrations [50 and 100 nM] of ArhGAP15 siRNA for 48 h respectively. Both concentrations of siRNA were effective and the results of RT-PCR revealed an efficient knock-down of ArhGAP15 mRNA in fibroblast cells. Further, the normal cells exposed to a 100 mM ethanol concentration showed a reduction in cell viability and induced the ratio of apoptosis related Bax/Bcl-2 proteins compared with ArhGAP15 siRNA transfected ethanol treated cells. Ethanol also increased caspase-3 expression in normal fibroblast cells compared with transfected cells. The ArhGAP15 knock-down cells treated with ethanol decreased Bax/Bcl-2 ratio and lower caspase-3 protein levels in ArhGAP15 knocked-down cells. Our results suggest that apoptosis induced by ethanol involves the activation of Rho GTPase activating protein 15 and silencing of the said gene protects apoptosis

Alien Hand Syndrome in Stroke: Case Report & Neurophysiologic Study

Alien Hand Syndrome is defined as unwilled, uncontrollable, but seemingly purposeful movements of an upper limb. Two major criteria for the diagnosis are complaint of a foreign limb and complex, autonomous, involuntary motor activity that is not part of an identifiable movement disorder. After a cerebrovascular accident in the corpus callosum, the parietal, or frontal regions, various abnormal involuntary motor behaviors may follow. Although different subtypes of Alien Hand Syndrome have been distinguished, this classification clearly does not cover the wide clinical variety of abnormal motor behaviors of the upper extremity. And there are few known studies about the neurophysiology of this syndrome using transcranial magnetic stimulation (TMS). We recently experienced 2 rare cases of Alien Hand Syndrome which occurred after anterior cerebral artery (ACA) infarction. A 72 year-old male with right hemiplegia following a left ACA infarct had difficulty with voluntarily releasing an object from his grasp. A 47 year-old female with left hemiplegia following a right ACA infarct had a problem termed 'intermanual conflict' in which the two hands appear to be directed at opposing purposes. Both of them had neurophysiologic studies done, and showed reduced amplitude by single pulse MEP and a lack of intracortical inhibition (ICI) by paired pulse TMS. No abnormalities were found in SSEP.