Cerebral Decortication
Thoracostomy
Chest Tubes
Collapse Therapy
Thoracic Surgical Procedures
Pleural Neoplasms
Pleura
Thoracic Surgery, Video-Assisted
Pleurisy
Agave
Instillation, Drug
Mesothelioma
Pulmonary Atelectasis
Debridement
Cerebral Infarction
Cerebral Palsy
Pleural Effusion
Middle Cerebral Artery
Visual responses of neurons in the middle temporal area of new world monkeys after lesions of striate cortex. (1/41)
In primates, lesions of striate cortex (V1) result in scotomas in which only rudimentary visual abilities remain. These aspects of vision that survive V1 lesions have been attributed to direct thalamic pathways to extrastriate areas, including the middle temporal area (MT). However, studies in New World monkeys and humans have questioned this interpretation, suggesting that remnants of V1 are responsible for both the activation of MT and residual vision. We studied the visual responses of neurons in area MT in New World marmoset monkeys in the weeks after lesions of V1. The extent of the scotoma in each case was estimated by mapping the receptive fields of cells located near the lesion border and by histological reconstruction. Two response types were observed among the cells located in the part of MT that corresponds, in visuotopic coordinates, to the lesioned part of V1. Many neurons (62%) had receptive fields that were displaced relative to their expected location, so that they represented the visual field immediately surrounding the scotoma. This may be a consequence of a process analogous to the reorganization of the V1 map after retinal lesions. However, another 20% of the cells had receptive fields centered inside the scotoma. Most of these neurons were strongly direction-selective, similar to normal MT cells. These results show that MT cells differ in their responses to lesioning of V1 and that only a subpopulation of MT neurons can be reasonably linked to residual vision and blindsight. (+info)Spiking-bursting activity in the thalamic reticular nucleus initiates sequences of spindle oscillations in thalamic networks. (2/41)
Recent intracellular and local field potential recordings from thalamic reticular (RE) neurons in vivo as well as computational modeling of the isolated RE nucleus suggest that, at relatively hyperpolarized levels of membrane potentials, the inhibitory postsynaptic potentials (IPSPs) between RE cells can be reversed and gamma-aminobutyric acid-A (GABA(A)) -mediated depolarization can generate persistent spatio-temporal patterns in the RE nucleus. Here we investigate how this activity affects the spatio-temporal properties of spindle oscillations with computer models of interacting RE and thalamocortical (TC) cells. In a one-dimensional network of RE and TC cells, sequences of spindle oscillations alternated with localized patterns of spike-burst activity propagating inside the RE network. New sequences of spindle oscillations were initiated after removal of I(h)-mediated depolarization of the TC cells. The length of the interspindle lulls depended on the intrinsic and synaptic properties of RE and TC cells and was in the range of 3-20 s. In a two-dimensional model, GABA(A)-mediated 2-3 Hz oscillations persisted in the RE nucleus during interspindle lulls and initiated spindle sequences at many foci within the RE-TC network simultaneously. This model predicts that the intrinsic properties of the reticular thalamus may contribute to the synchrony of spindle oscillations observed in vivo. (+info)Emotional cognition without awareness after unilateral temporal lobectomy in humans. (3/41)
To investigate the function of the amygdala in human emotional cognition, we investigated the electrodermal activity (EDA) in response to masked (unseen) visual stimuli. Six epileptic subjects were investigated after unilateral temporal lobectomy. Emotionally valenced photographic slides (10 negative, 10 neutral) from the International Affective Picture System were presented to their unilateral visual fields under either subliminal or supraliminal conditions. An interaction between hemispheres and emotional valences was found only under the subliminal conditions; greater EDA responses to negative stimuli compared with neutral ones were observed when stimuli were presented to the intact hemispheres. The findings suggest that nonconscious emotional processing is reflected in EDA in a different manner from conscious emotional processing. Medial temporal structures, including the amygdala, thus appear to play a critical role in the neural substrates for this automatic processing. (+info)Dissociable roles of mid-dorsolateral prefrontal and anterior inferotemporal cortex in visual working memory. (4/41)
Functional neuroimaging in human subjects and studies of monkeys with lesions limited to the mid-dorsolateral (MDL) prefrontal cortex have shown that this specific region of the prefrontal cortex is involved in visual working memory, although its precise role remains a matter of debate. The present study compared the effect on visual working memory of lesions restricted to the mid-dorsolateral prefrontal cortex of the monkey with that of lesions to the anterior inferotemporal cortex, a region of the temporal cortex specialized for visual memory. Increasing the delay during which information had to be maintained in visual working memory impaired performance after lesions of the anterior inferotemporal cortex, but not after mid-dorsolateral prefrontal lesions. By contrast, increasing the number of stimuli that had to be monitored impaired the performance of animals with mid-dorsolateral prefrontal lesions, but not that of animals with anterior inferotemporal lesions. This demonstration of a double dissociation between the effects of these two lesions provides strong evidence that the role of the mid-dorsolateral prefrontal cortex in visual working memory does not lie in the maintenance of information per se, but rather in the executive process of monitoring this information. In addition, the present study demonstrated that lesions limited to area 9, which constitutes the superior part of the mid-dorsolateral prefrontal region, give rise to a mild impairment in the monitoring of information, whereas lesions of the complete mid-dorsolateral prefrontal region yield a very severe impairment. (+info)The reorganization of sensorimotor function in children after hemispherectomy. A functional MRI and somatosensory evoked potential study. (5/41)
Children who have suffered extensive unilateral brain injury early in life may show a remarkable degree of residual sensorimotor function. It is generally believed that this reflects the high capacity of the immature brain for cerebral reorganization. In this study, we investigated 17 patients who had undergone hemispherectomy for relief from seizures; eight of the patients had congenital brain damage and nine had sustained their initial insult at the age of 1 year or older. Sensorimotor functions of the hand were investigated using functional MRI (fMRI) during a passive movement task, somatosensory evoked potentials (SEPs) arising from electrical and vibration stimulation, and behavioural tests including grip strength, double simultaneous stimulation and joint position sense. On fMRI, two of the eight patients studied with this technique (one with congenital damage and one with damage acquired at the age of 3 years) showed activation in the sensorimotor cortex of the remaining hemisphere with passive movement of the hemiplegic hand. The location of the ipsilateral brain activation was similar to that found on movement of the normal contralateral hand, although the latter was greater in spatial extent. In one of these patients, a greater role was demonstrated for the ipsilateral secondary sensorimotor area (compared with the ipsilateral primary sensorimotor area) for movement of the hemiplegic hand than for movement of the normal hand. Median nerve stimulation of the hemiplegic hand showed reproducible early-latency ipsilateral SEP components in the remaining sensorimotor cortex in 10 of the 17 patients (five with congenital and five with acquired disease). Five of the patients who demonstrated ipsilateral electrical SEPs also showed ipsilateral vibration SEPs (two with congenital and three with acquired disease). The behavioural tests revealed residual sensorimotor function in 14 of the patients; however, not all of the patients who exhibited ipsilateral SEP or fMRI responses had residual sensorimotor function in the hemiplegic hand. Ipsilateral sensorimotor responses were demonstrated both in patients with congenital disease and those with acquired disease, suggesting that factors additional to aetiology and age at injury may influence the degree of residual sensorimotor function and cerebral reorganization. (+info)Failed surgery for epilepsy. A study of persistence and recurrence of seizures following temporal resection. (6/41)
From a series of 282 consecutive temporal resections for medically intractable epilepsy associated with mesial temporal sclerosis (MTS), dysembryoplastic neuroepithelial tumour (DNT) or non-specific pathology (NSP), 51 patients had persistent or recurrent seizures occurring at least monthly. Of these patients, 44 underwent detailed assessment of their postoperative seizures, which included clinical evaluation, interictal and ictal EEG and high-resolution MRI. Of the 20 patients with MTS in the original pathology, 14 (70%) had postoperative seizures arising in the hemisphere of the resection, the majority (12 patients) in the temporal region. Although MRI demonstrated residual hippocampus in five of these 12 patients, only one patient was considered to have seizures arising there, whilst the remainder had electroclinical evidence of seizure onset in the neocortex. In contrast, five of the MTS relapses (25%) had seizure onset exclusively in the contralateral temporal region. Among the 14 patients with non-specific pathology, relapse was also predominantly from the ipsilateral hemisphere (64%), but more relapsed from extratemporal sites compared with the MTS cases, including two with NSP who had occipital structural abnormalities. Although 70% of the 10 patients with DNT had postoperative partial seizures arising in the ipsilateral hemisphere, many (60%) had evidence of a more diffuse disorder with additional generalized seizures, cognitive and behavioural disturbance and multifocal and generalized EEG abnormalities. Nine patients (20%) had immediate postoperative seizure-free periods of at least 1 year, and seven of these had MTS in the operative specimen. Of these seven patients, four had ipsilateral temporal seizures and three had contralateral temporal seizures. Overall, few missed lesions were discovered on postoperative MRI and reoperations were performed or considered possible in a minority of cases. Despite well-defined preoperative electroclinical syndromes of temporal lobe epilepsy, many patients relapsed unexpectedly, either immediately or remotely from the time of surgery. Maturing epileptogenicity in a surgical scar was not, however, considered to be a significant primary mechanism in patients who relapsed after a seizure-free interval. (+info)Chronic NMDA receptor blockade from birth increases the sprouting capacity of ipsilateral retinocollicular axons without disrupting their early segregation. (7/41)
We have investigated the role of the NMDA glutamate receptor (NMDAR) in the genesis and regulation of structural plasticity during synaptogenesis in the visual layers of the rat superior colliculus (sSC). In this neuropil, three projections compete for synaptic space during development. By fluorescently labeling the projections of both eyes and imaging them with confocal microscopy, we can quantify the sprouting of the ipsilateral retinal projection that follows removal of a portion of the contralateral retinal and/or corticocollicular projection. Using these techniques we have studied the effects of NMDAR blockade under different levels of competition. NMDARs were chronically blocked from birth [postnatal day 0 (P0)] by suspending the competitive antagonist 2-amino-5-phosphonopentanoic acid in the slow release plastic Elvax, a slab of which was implanted over the sSC. Such treatment alone does not impair the normal segregation of the retinal projections. However, if sprouting of the ipsilateral projection is initiated with a small contralateral retinal lesion at P6, this sprouting can be further increased by blocking NMDARs from birth. Sprouting of the ipsilateral retinal projection is also induced by retinal lesions made at P10/P11, but NMDAR blockade does not augment the sprouting induced by this later lesion. However, when combined with simultaneous ablation of the ipsilateral visual cortex, P10/P11 lesions show increased sprouting after NMDAR blockade. These data indicate that P0 NMDAR blockade does not eliminate synaptic competition in the sSC. Instead, early elimination of NMDAR function appears to facilitate sprouting that is gated in a stepwise manner by the other visual afferents. (+info)Specific force of the rat extraocular muscles, levator and superior rectus, measured in situ. (8/41)
Extraocular muscles are characterized by their faster rates of contraction and their higher resistance to fatigue relative to limb skeletal muscles. Another often reported characteristic of extraocular muscles is that they generate lower specific forces (sP(o), force per muscle cross-sectional area, kN/m(2)) than limb skeletal muscles. To investigate this perplexing issue, the isometric contractile properties of the levator palpebrae superioris (levator) and superior rectus muscles of the rat were examined in situ with nerve and blood supply intact. The extraocular muscles were attached to a force transducer, and the cranial nerves exposed for direct stimulation. After determination of optimal muscle length (L(o)) and stimulation voltage, a full frequency-force relationship was established for each muscle. Maximum isometric tetanic force (P(o)) for the levator and superior rectus muscles was 177 +/- 13 and 280 +/- 10 mN (mean +/- SE), respectively. For the calculation of specific force, a number of rat levator and superior rectus muscles were stored in a 20% nitric acid-based solution to isolate individual muscle fibers. Muscle fiber lengths (L(f)) were expressed as a percentage of overall muscle length, allowing a mean L(f) to L(o) ratio to be used in the estimation of muscle cross-sectional area. Mean L(f):L(o) was determined to be 0.38 for the levator muscle and 0.45 for the superior rectus muscle. The sP(o) for the rat levator and superior rectus muscles measured in situ was 275 and 280 kN/m(2), respectively. These values are within the range of sP(o) values commonly reported for rat skeletal muscles. Furthermore P(o) and sP(o) for the rat levator and superior rectus muscles measured in situ were significantly higher (P < 0.001) than P(o) and sP(o) for these muscles measured in vitro. The results indicate that the force output of intact extraocular muscles differs greatly depending on the mode of testing. Although in vitro evaluation of extraocular muscle contractility will continue to reveal important information about this group of understudied muscles, the lower sP(o) values of these preparations should be recognized as being significantly less than their true potential. We conclude that extraocular muscles are not intrinsically weaker than skeletal muscles. (+info)[Term]
Empyema, Pleural
[Definition]
A condition characterized by the accumulation of pus in the pleural space between the lungs and chest wall, caused by bacterial infection or other inflammatory conditions. Symptoms include fever, chest pain, coughing, and difficulty breathing. Treatment involves antibiotics, drainage of pus, and supportive care.
[Origin]
From the Greek words "empyema" meaning "into the pleura" and "pleural" referring to the space between the lungs and chest wall.
[Types]
There are several types of empyema, including:
1. Pyogenic empyema: caused by bacterial infection, most commonly with Staphylococcus aureus.
2. Tubercular empyema: caused by tuberculosis infection.
3. Cat-scratch empyema: caused by bacteria entering the pleural space through a scratch or wound.
4. Hemorrhagic empyema: caused by bleeding into the pleural space.
[Symptoms]
Symptoms of empyema may include:
1. Fever
2. Chest pain that worsens with deep breathing or coughing
3. Coughing up pus or blood
4. Difficulty breathing
5. Fatigue
6. Loss of appetite
[Diagnosis]
Empyema is diagnosed through a combination of physical examination, chest x-ray, and pleural fluid analysis. A chest x-ray can confirm the presence of pus in the pleural space, while pleural fluid analysis can identify the type of bacteria or other infectious agents present.
[Treatment]
Treatment of empyema typically involves antibiotics to eradicate the underlying infection and drainage of the pleural fluid. In some cases, surgical intervention may be necessary to remove infected tissue or repair damaged lung tissue.
[Prognosis]
The prognosis for empyema depends on the severity of the infection and the promptness and effectiveness of treatment. With prompt and appropriate treatment, the majority of patients with empyema can recover fully. However, delays in diagnosis and treatment can lead to serious complications, including respiratory failure, sepsis, and death.
[Prevention]
Preventing the development of empyema requires prompt and effective management of underlying conditions such as pneumonia, tuberculosis, or other respiratory infections. Vaccination against Streptococcus pneumoniae and other bacteria that can cause empyema may also be recommended.
[Conclusion]
Empyema is a potentially life-threatening condition that requires prompt and appropriate treatment to prevent serious complications and improve outcomes. Awareness of the risk factors, symptoms, diagnosis, and treatment options for empyema can help healthcare providers provide effective care for patients with this condition.
Empyema can be classified into two types:
1. Pyopneumothorax: This type of empyema is caused by a bacterial infection that spreads to the pleural space and causes pus to accumulate.
2. Chemical pneumonitis: This type of empyema is caused by exposure to chemical irritants, such as smoke or chemical fumes, which can damage the lungs and cause inflammation and pus accumulation in the pleural space.
Symptoms of empyema may include chest pain, fever, coughing up pus, and difficulty breathing. Treatment options for empyema depend on the severity of the condition and may include antibiotics, chest tubes, or surgery to drain the pus from the pleural space.
Empyema is a serious medical condition that can lead to complications such as respiratory failure, sepsis, and lung damage if left untreated. Prompt diagnosis and treatment are essential to prevent these complications and improve outcomes for patients with empyema.
TB empyema is a rare complication of pulmonary TB, occurring in approximately 1-5% of all cases of pulmonary TB. It is more common in immunocompromised individuals, such as those with HIV/AIDS or those taking immunosuppressive medications following organ transplantation.
The symptoms of TB empyema may include cough, fever, chest pain, difficulty breathing, and fatigue. The diagnosis is typically made through a combination of chest radiography, computed tomography (CT) scans, and microbiological tests such as sputum smears or cultures.
Treatment of TB empyema typically involves a combination of antituberculous medications and drainage of the purulent material. In some cases, surgical intervention may be necessary to remove the infected tissue. Treatment outcomes are generally good if the diagnosis is made early and appropriate therapy is initiated promptly. However, delays in diagnosis and treatment can lead to serious complications such as respiratory failure, sepsis, and death.
Benign pleural neoplasms include:
1. Pleomorphic adenoma: A rare, slow-growing tumor that usually occurs in the soft tissues of the chest wall.
2. Pneumoschisis: A condition where there is a tear or separation in the membrane that lines the lung, which can cause air to leak into the pleural space and create a benign tumor.
3. Pleural plaques: Calcified deposits that form in the pleura as a result of inflammation or injury.
Malignant pleural neoplasms include:
1. Mesothelioma: A rare and aggressive cancer that originates in the pleura, usually caused by exposure to asbestos.
2. Lung cancer: Cancer that spreads to the pleura from another part of the body, such as the lungs.
3. Metastatic tumors: Tumors that have spread to the pleura from another part of the body, such as the breast or colon.
Pleural neoplasms can cause a variety of symptoms, including chest pain, shortness of breath, coughing, and fatigue. Diagnosis is typically made through a combination of imaging tests, such as CT scans and PET scans, and a biopsy to confirm the presence of cancerous cells. Treatment options for pleural neoplasms depend on the type and stage of the tumor, and may include surgery, chemotherapy, and radiation therapy.
Some common types of pleural diseases include:
1. Pleurisy: This is an inflammation of the pleura that can be caused by infection, injury, or cancer. Symptoms include chest pain, fever, and difficulty breathing.
2. Pneumothorax: This is a collection of air or gas between the pleural membranes that can cause the lung to collapse. Symptoms include sudden severe chest pain, shortness of breath, and coughing up blood.
3. Empyema: This is an infection of the pleural space that can cause the accumulation of pus and fluid. Symptoms include fever, chills, and difficulty breathing.
4. Mesothelioma: This is a type of cancer that affects the pleura and can cause symptoms such as chest pain, shortness of breath, and weight loss.
5. Pleural effusion: This is the accumulation of fluid in the pleural space that can be caused by various conditions such as infection, heart failure, or cancer. Symptoms include chest pain, shortness of breath, and coughing up fluid.
Pleural diseases can be diagnosed through various tests such as chest X-rays, CT scans, and pleuroscopy (a minimally invasive procedure that uses a thin tube with a camera and light on the end to examine the pleura). Treatment options vary depending on the underlying cause of the disease and can include antibiotics, surgery, or radiation therapy.
The symptoms of mesothelioma can vary depending on the location of the cancer, but they may include:
* Shortness of breath or pain in the chest (for pleural mesothelioma)
* Abdominal pain or swelling (for peritoneal mesothelioma)
* Fatigue or fever (for pericardial mesothelioma)
* Weight loss and night sweats
There is no cure for mesothelioma, but treatment options may include surgery, chemotherapy, and radiation therapy. The prognosis for mesothelioma is generally poor, with a five-year survival rate of about 5% to 10%. However, the outlook can vary depending on the type of mesothelioma, the stage of the cancer, and the patient's overall health.
Asbestos exposure is the primary risk factor for developing mesothelioma, and it is important to avoid exposure to asbestos in any form. This can be done by avoiding old buildings and products that contain asbestos, wearing protective clothing and equipment when working with asbestos, and following proper safety protocols when handling asbestos-containing materials.
In summary, mesothelioma is a rare and aggressive form of cancer that develops in the lining of the heart or abdomen due to exposure to asbestos. It can be difficult to diagnose and treat, and the prognosis is generally poor. However, with proper medical care and avoidance of asbestos exposure, patients with mesothelioma may have a better chance of survival.
Symptoms of pulmonary atelectasis may include chest pain, coughing up bloody mucus, difficulty breathing, fever, and chills. Treatment typically involves antibiotics for bacterial infections, and in severe cases, mechanical ventilation may be necessary. In some cases, surgery may be required to remove the blockage or repair the damage to the lung.
Pulmonary atelectasis is a serious condition that requires prompt medical attention to prevent complications such as respiratory failure or sepsis. It can be diagnosed through chest X-rays, computed tomography (CT) scans, and pulmonary function tests.
Cerebral infarction can result in a range of symptoms, including sudden weakness or numbness in the face, arm, or leg on one side of the body, difficulty speaking or understanding speech, sudden vision loss, dizziness, and confusion. Depending on the location and severity of the infarction, it can lead to long-term disability or even death.
There are several types of cerebral infarction, including:
1. Ischemic stroke: This is the most common type of cerebral infarction, accounting for around 87% of all cases. It occurs when a blood clot blocks the flow of blood to the brain, leading to cell death and tissue damage.
2. Hemorrhagic stroke: This type of cerebral infarction occurs when a blood vessel in the brain ruptures, leading to bleeding and cell death.
3. Lacunar infarction: This type of cerebral infarction affects the deep structures of the brain, particularly the basal ganglia, and is often caused by small blockages or stenosis (narrowing) in the blood vessels.
4. Territorial infarction: This type of cerebral infarction occurs when there is a complete blockage of a blood vessel that supplies a specific area of the brain, leading to cell death and tissue damage in that area.
Diagnosis of cerebral infarction typically involves a combination of physical examination, medical history, and imaging tests such as CT or MRI scans. Treatment options vary depending on the cause and location of the infarction, but may include medication to dissolve blood clots, surgery to remove blockages, or supportive care to manage symptoms and prevent complications.
Causes:
1. Brain injury during fetal development or birth
2. Hypoxia (oxygen deficiency) to the brain, often due to complications during labor and delivery
3. Infections such as meningitis or encephalitis
4. Stroke or bleeding in the brain
5. Traumatic head injury
6. Genetic disorders
7. Premature birth
8. Low birth weight
9. Multiples (twins, triplets)
10. Maternal infections during pregnancy.
Symptoms:
1. Weakness or paralysis of muscles on one side of the body
2. Lack of coordination and balance
3. Difficulty with movement, posture, and gait
4. Spasticity (stiffness) or hypotonia (looseness) of muscles
5. Intellectual disability or learning disabilities
6. Seizures
7. Vision, hearing, or speech problems
8. Swallowing difficulties
9. Increased risk of infections and bone fractures
10. Delays in reaching developmental milestones.
Diagnosis:
1. Physical examination and medical history
2. Imaging tests, such as CT or MRI scans
3. Electromyography (EMG) to test muscle activity
4. Developmental assessments to evaluate cognitive and motor skills
5. Genetic testing to identify underlying causes.
Treatment:
1. Physical therapy to improve movement, balance, and strength
2. Occupational therapy to develop daily living skills and fine motor activities
3. Speech therapy for communication and swallowing difficulties
4. Medications to control seizures, spasticity, or pain
5. Surgery to correct anatomical abnormalities or release contracted muscles
6. Assistive devices, such as braces, walkers, or wheelchairs, to aid mobility and independence.
It's important to note that each individual with Cerebral Palsy may have a unique combination of symptoms and require a personalized treatment plan. With appropriate medical care and support, many individuals with Cerebral Palsy can lead fulfilling lives and achieve their goals despite the challenges they face.