High Pressure Neurological Syndrome
Paraneoplastic Syndromes, Nervous System
Paraneoplastic Polyneuropathy
Paraneoplastic Cerebellar Degeneration
Stiff-Person Syndrome
Nervous System Diseases
Transcatheter closure of patent foramen ovale using the Amplatzer septal occluder to prevent recurrence of neurological decompression illness in divers. (1/8)
OBJECTIVE: Large flap valve patent foramens may cause paradoxical thromboembolism and neurological decompression illness in divers. The ability of a self expanding Nitinol wire mesh device (Amplatzer septal occluder) to produce complete closure of the patent foramen ovale was assessed. PATIENTS: Seven adults, aged 18-60 years, who had experienced neurological decompression illness related to diving. Six appeared to have a normal atrial septum on transthoracic echocardiography, while one was found to have an aneurysm of the interatrial septum. METHODS: Right atrial angiography was performed to delineate the morphology of the right to left shunt. The defects were sized bidirectionally with a precalibrated balloon filled with dilute contrast. The largest balloon diameter that could be repeatedly passed across the septum was used to select the occlusion device diameter. Devices were introduced through 7 F long sheaths. All patients underwent transthoracic contrast echocardiography one month after the implant. RESULTS: Device placement was successful in all patients. Device sizes ranged from 9-14 mm. The patient with an aneurysm of the interatrial septum had three defects, which were closed with two devices. Right atrial angiography showed complete immediate closure in all patients. Median (range) fluoroscopy time was 13.7 (6-35) minutes. Follow up contrast echocardiography showed no right to left shunting in six of seven patients and the passage of a few bubbles in one patient. All patients have been allowed to return to diving. CONCLUSION: The Amplatzer septal occluder can close the large flap valve patent foramen ovale in divers who have experienced neurological decompression illness. Interatrial septal aneurysms with multiple defects may require more than one device. (+info)Pressure (< or=4 ATA) increases membrane conductance and firing rate in the rat solitary complex. (2/8)
Neuronal sensitivity to pressure, barosensitivity, is illustrated by high-pressure nervous syndrome, which manifests as increased central nervous system excitability when heliox or trimix is breathed at >15 atmospheres absolute (ATA). We have tested the hypothesis that smaller levels of pressure (Modulation of rat corticohippocampal synaptic activity by high pressure and extracellular calcium: single and frequency responses. (3/8)
High pressure (>1.5 MPa) induces a series of disturbances of the nervous system that are generically termed high-pressure nervous syndrome (HPNS). HPNS is characterized by motor and cognitive impairments. The neocortex and the hippocampus are presumably involved in this last disorder. The medial perforant path (MPP) synapse onto the granule cells of the dentate gyrus is the main connection between these structures. We have studied high-pressure (HP) effects on single and frequency response of this synapse. Since effects of HP on various synapses were mimicked by reducing [Ca2+]o, results under these conditions were compared. Medial perforant path-evoked field excitatory postsynaptic potentials (fEPSPs) were recorded from granule cells in rat brain slices. Slices were exposed to high pressure of helium (0.1-10.1 MPa) at 30 degrees C. HP depressed single fEPSPs by 35 and 55% at 5.1 and 10.1 MPa, respectively, and increased paired-pulse facilitation (PPF) at 10- to 40-ms inter-stimulus intervals. Frequency-dependent depression (FDD) was enhanced by HP during trains of stimuli at 50 but not at 25 Hz. Depression of single fEPSPs by reduction of [Ca2+]o from 2 mM control to 1 mM at normal pressure was equivalent to the effect of 10.1 MPa at control [Ca2+]o. However, this low [Ca2+]o induced greater enhancement of PPF, and in contrast, turned FDD at 25-50 Hz into frequency-dependent potentiation. These results suggest that HP depresses single synaptic release by reducing Ca2+ entry, whereas slowing of synaptic frequency response is independent of Ca2+. These findings increase our understanding of HPNS experienced by deep divers. (+info)Neurological long term consequences of deep diving. (4/8)
Forty commercial saturation divers, mean age 34.9 (range 24-49) years, were examined one to seven years after their last deep dive (190-500 metres of seawater). Four had by then lost their divers' licence because of neurological problems. Twenty seven (68%) had been selected by neurological examination and electroencephalography before the deep dives. The control group consisted of 100 men, mean age 34.0 (range 22-48) years. The divers reported significantly more symptoms from the nervous system. Concentration difficulties and paraesthesia in feet and hands were common. They had more abnormal neurological findings by neurological examination compatible with dysfunction in the lumbar spinal cord or roots. They also had a larger proportion of abnormal electroencephalograms than the controls. The neurological symptoms and findings were highly significantly correlated with exposure to deep diving (depth included), but even more significantly correlated to air and saturation diving and prevalence of decompression sickness. Visual evoked potentials, brainstem auditory evoked potentials, and magnetic resonance imaging of the brain did not show more abnormal findings in the divers. Four (10%) divers had had episodes of cerebral dysfunction during or after the dives; two had had seizures, one had had transitory cerebral ischaemia and one had had transitory global amnesia. It is concluded that deep diving may have a long term effect on the nervous system of the divers. (+info)Systemically administered glycine protects against strychnine convulsions, but not the behavioural effects of high pressure, in mice. (5/8)
1. The effects of intraperitoneal administration of glycine were studied on the behavioural effects of raised ambient pressure in mice, compared with the effects of such administration on the actions of chemical convulsants. 2. Glycine did not alter the onset pressures for the occurrence of tremor, myoclonic jerks or clonic convulsions, when the ambient pressure was raised using helium. 3. Glycine showed a protective action against the convulsant effects of strychnine. 4. No protective action of glycine was found against the convulsant actions of pentylenetetrazol or bicuculline. 5. It is suggested that the results provide evidence that the high pressure neurological syndrome and strychnine convulsions have different neurophysiological origins. (+info)Possible NMDA antagonist properties of drugs that affect high pressure neurological syndrome. (6/8)
1. Previous studies have suggested that a series of drugs modelled on part of the strychnine molecule interfere with the development of high pressure neurological syndrome (HPNS) and it was presumed that this effect was via an action on inhibitory glycinergic transmission. We have now used the rat hippocampal slice preparation to examine the possibility that some of these drugs might instead have an action at the strychnine-insensitive (SI) glycine binding site associated with the NMDA receptor. 2. D-2-Amino-5-phosphonovalerate (AP5) and 7-chlorokynurenate (7CK) had no significant effect on the height of the population spike recorded from the CA1 region in 1 mM Mg2+ medium, but both blocked the multiple population spikes recorded in Mg(2+)-free medium. The effect of 7CK, but not AP5, was reversed by 200 microM D-serine which is consistent with the known antagonist action of 7CK at the SI-glycine site. 3. A derivative of benzimidazole, which shows the clearest structural similarities to known SI-glycine site antagonists and ameliorates HPNS, mirrored the effects of 7CK although it was considerably less potent. 4. Gramine, which exacerbates HPNS, significantly increased the number of population spikes evoked in Mg(2+)-free medium. 5. Mephenesin, which is the most potent known drug in ameliorating HPNS, had no significant effect on the response recorded in 1 mM Mg2+ and significantly reduced the number of population spikes recorded in Mg(2+)-free medium, but this effect was only partially reversed by the addition of D-serine. 6. The results are consistent with the benzimidazole derivative, but not gramine, being an antagonist at the SI-glycine receptor. The results with mephenesin are equivocal but leave open the possibility that some of the drugs which are effective against HPNS act via an effect on excitatory NMDA receptor mediated transmission, rather than on inhibitory glycine-mediated transmission. (+info)EEG and sleep disturbances during dives at 450 msw in helium-nitrogen-oxygen mixture. (7/8)
To study the effects of nitrogen addition to the breathing mixture on sleep disturbances at pressure, two dives were performed in which helium-nitrogen-oxygen mixture was used up to 450 m sea water (msw). In total, sleep of 12 professional divers was analyzed (i.e., 184 night records). Sleep was disrupted by compression and by stay at 450 msw: we observed an increase in awake periods and in sleep stages I and II and a decrease in stages III and IV and in rapid-eye-movement sleep periods. These changes, which were more intense at the beginning of the stay, began to decrease from the seventh day of the stay, but the return to control values was recorded only during the decompression at depths below 200 msw. These changes were equivalent to those recorded in other experiments with helium-oxygen mixture in the same range of depths and were independent of the intensity of changes recorded in electroencephalographic activities in awake subjects. (+info)Relationship between T-wave amplitude and oxygen pulse in guinea pigs in hyperbaric helium and hydrogen. (8/8)
Diving is known to induce a change in the amplitude of the T wave (ATw) of electrocardiograms, but it is unknown whether this is linked to a change in cardiovascular performance. We analyzed ATw in guinea pigs at 10-60 atm and 25-36 degreesC, breathing 2% O2 in either helium (heliox; n = 10) or hydrogen (hydrox; n = 9) for 1 h at each pressure. Core temperature and electrocardiograms were detected by using implanted radiotelemeters. O2 consumption rate was measured by using gas chromatography. In a previous study (S. R. Kayar and E. C. Parker. J. Appl. Physiol. 82: 988-997, 1997), we analyzed the O2 pulse, i.e., the O2 consumption rate per heart beat, in the same animals. By multivariate regression analysis, we identified variables that were significant to O2 pulse: body surface area, chamber temperature, core temperature, and pressure. In this study, inclusion of ATw made a significantly better model with fewer variables. After normalizing for chamber temperature and pressure, the O2 pulse increased with increasing ATw in heliox (P = 0.001) but with decreasing ATw in hydrox (P < 0.001). Thus ATw is associated with the differences in O2 pulse for animals breathing heliox vs. hydrox. (+info)High pressure neurological syndrome (HPNS) is not a specific medical condition but rather a group of symptoms that can occur in deep sea divers during rapid decompression or ascent from great depths. It is caused by the increased pressure of nitrogen gas dissolved in the blood and tissues, which can affect the nervous system and cause various neurological symptoms.
HPNS is characterized by a range of symptoms including tremors, myoclonic jerks (involuntary muscle twitches), visual disturbances, nausea, dizziness, disorientation, and decreased mental performance. In severe cases, it can lead to seizures, loss of consciousness, and even death.
The exact mechanisms underlying HPNS are not fully understood, but it is believed that the high pressure causes changes in the membranes of nerve cells, leading to altered ion channel function and neurotransmitter release. The symptoms of HPNS can be minimized by using a slow decompression rate or by using gas mixtures that reduce the amount of nitrogen in the breathing gas.
Mephenesin is a muscle relaxant that has been used in the past to treat various conditions such as spasticity and muscle pain. It works by blocking nerve impulses that are sent to the muscles, which helps to reduce muscle tension and spasms. However, mephenesin is not commonly used today due to its potential for abuse and the availability of safer and more effective muscle relaxants.
Mephenesin is a carbamate derivative and acts as a central nervous system depressant. It has sedative and hypnotic effects, which can make it useful in managing anxiety and promoting sleep. However, mephenesin can also cause respiratory depression, especially when used in high doses or in combination with other central nervous system depressants.
Mephenesin is available in various forms, including tablets, capsules, and injectable solutions. It is important to follow the prescribed dosage carefully and to avoid using mephenesin with alcohol or other drugs that can cause drowsiness or respiratory depression. Side effects of mephenesin may include dizziness, headache, nausea, vomiting, and skin rash. In rare cases, mephenesin can cause more serious side effects such as seizures, coma, and death.
Paraneoplastic syndromes of the nervous system are a group of rare disorders that occur in some individuals with cancer. These syndromes are caused by an immune system response to the cancer tumor, which can lead to the damage or destruction of nerve cells. The immune system produces antibodies and/or activated immune cells that attack the neural tissue, leading to neurological symptoms.
Paraneoplastic syndromes can affect any part of the nervous system, including the brain, spinal cord, peripheral nerves, and muscles. Symptoms vary depending on the specific syndrome and the location of the affected nerve tissue. Some common neurological symptoms include muscle weakness, numbness or tingling, seizures, memory loss, confusion, difficulty speaking or swallowing, visual disturbances, and coordination problems.
Paraneoplastic syndromes are often associated with specific types of cancer, such as small cell lung cancer, breast cancer, ovarian cancer, and lymphoma. Diagnosis can be challenging because the symptoms may precede the discovery of the underlying cancer. A combination of clinical evaluation, imaging studies, laboratory tests, and sometimes a brain biopsy may be necessary to confirm the diagnosis.
Treatment typically involves addressing the underlying cancer with surgery, chemotherapy, or radiation therapy. Immunosuppressive therapies may also be used to manage the immune response that is causing the neurological symptoms. While treatment can help alleviate symptoms and improve quality of life, paraneoplastic syndromes are often difficult to cure completely.
Paraneoplastic polyneuropathy is a rare neurological disorder that can occur in some individuals with cancer. It's caused by the immune system producing antibodies or cells that attack the nervous system (neurons, nerve axons, or myelin sheath) as a response to the presence of a tumor or cancer in the body.
The term "polyneuropathy" refers to damage or dysfunction affecting multiple peripheral nerves simultaneously. This can lead to various symptoms such as numbness, tingling, muscle weakness, and pain, typically starting in the hands and feet and progressing upwards.
In paraneoplastic polyneuropathy, these symptoms are related to the immune system's response to the cancer rather than direct invasion of the nerves by the tumor itself. The specific type of polyneuropathy can vary between individuals, and it may present as sensorimotor polyneuropathy, autonomic neuropathy, or a combination of both.
Early diagnosis and treatment of the underlying cancer are crucial for managing paraneoplastic polyneuropathy. Immunotherapy, plasma exchange, and intravenous immunoglobulin may be used to help control the immune response and alleviate symptoms.
Paraneoplastic cerebellar degeneration (PCD) is a rare disorder characterized by progressive damage to the cerebellum, the part of the brain responsible for coordinating muscle movements. It is considered a paraneoplastic syndrome, which means it is caused by an abnormal immune system response to a cancerous tumor (neoplasm) located elsewhere in the body.
In PCD, antibodies produced by the immune system to fight the tumor mistakenly attack proteins in the cerebellum that are similar to those found in the tumor. This leads to inflammation and degeneration of the Purkinje cells, a type of neuron critical for maintaining balance and coordinating movements.
PCD can present with symptoms such as unsteady gait, loss of coordination, slurred speech, nystagmus (involuntary eye movement), and tremors. These symptoms often develop rapidly, over the course of days to weeks, and may progress even after the tumor has been removed or treated.
PCD is associated with several types of cancers, including small cell lung cancer, breast cancer, ovarian cancer, Hodgkin's lymphoma, and others. Early diagnosis and treatment of the underlying cancer are essential to slowing down the progression of PCD and improving outcomes.
A syndrome, in medical terms, is a set of symptoms that collectively indicate or characterize a disease, disorder, or underlying pathological process. It's essentially a collection of signs and/or symptoms that frequently occur together and can suggest a particular cause or condition, even though the exact physiological mechanisms might not be fully understood.
For example, Down syndrome is characterized by specific physical features, cognitive delays, and other developmental issues resulting from an extra copy of chromosome 21. Similarly, metabolic syndromes like diabetes mellitus type 2 involve a group of risk factors such as obesity, high blood pressure, high blood sugar, and abnormal cholesterol or triglyceride levels that collectively increase the risk of heart disease, stroke, and diabetes.
It's important to note that a syndrome is not a specific diagnosis; rather, it's a pattern of symptoms that can help guide further diagnostic evaluation and management.
Stiff-Person Syndrome (SPS) is a rare neurological disorder characterized by fluctuating muscle rigidity in the trunk and limbs and a heightened sensitivity to stimuli such as touch, sound, and emotional distress, which can trigger muscle spasms. The symptoms can significantly affect a person's ability to perform daily activities and can lead to frequent falls and injuries. SPS is often associated with antibodies against glutamic acid decarboxylase (GAD), an enzyme involved in the production of a neurotransmitter called gamma-aminobutyric acid (GABA) that helps regulate muscle movement. The exact cause of SPS remains unknown, but it is thought to involve both autoimmune and genetic factors.
Nervous system diseases, also known as neurological disorders, refer to a group of conditions that affect the nervous system, which includes the brain, spinal cord, nerves, and muscles. These diseases can affect various functions of the body, such as movement, sensation, cognition, and behavior. They can be caused by genetics, infections, injuries, degeneration, or tumors. Examples of nervous system diseases include Alzheimer's disease, Parkinson's disease, multiple sclerosis, epilepsy, migraine, stroke, and neuroinfections like meningitis and encephalitis. The symptoms and severity of these disorders can vary widely, ranging from mild to severe and debilitating.
Paraneoplastic syndromes refer to a group of rare disorders that are caused by an abnormal immune system response to a cancerous (malignant) tumor. These syndromes are characterized by symptoms or signs that do not result directly from the growth of the tumor itself, but rather from substances produced by the tumor or the body's immune system in response to the tumor.
Paraneoplastic syndromes can affect various organs and systems in the body, including the nervous system, endocrine system, skin, and joints. Examples of paraneoplastic syndromes include Lambert-Eaton myasthenic syndrome (LEMS), which affects nerve function and causes muscle weakness; cerebellar degeneration, which can cause difficulty with coordination and balance; and dermatomyositis, which is an inflammatory condition that affects the skin and muscles.
Paraneoplastic syndromes can occur in association with a variety of different types of cancer, including lung cancer, breast cancer, ovarian cancer, and lymphoma. Treatment typically involves addressing the underlying cancer, as well as managing the symptoms of the paraneoplastic syndrome.