Inhibitory Postsynaptic Potentials
Cerebellar afferents from neurons in the extraocular motor nuclei: a fluorescent retrograde double-labeling study in the sheep. (1/323)The fluorescent retrograde double labeling technique has been used to identify within the extraocular motor nuclei of the sheep the neurons projecting to the cerebellum and to provide evidence whether they are motor neurons sending collaterals to the cerebellum or a separate population of neurons. The study was performed on eight sheep. The fluorescent tracers used were Fast Blue and the diamidino yellow dihydrochloride. In one and the same animal a fluorescent tracer was injected into the extraocular muscles (EOMs) and the other into bilateral points of the vermal folia II-V and paramedian lobule, or into the vermal folia VI, VIIA and VIIB, or into the underlying fastigial nuclei. Within the oculomotor, trochlear, and abducens nuclei, almost all of the motor neurons were labeled by the tracer injected into the EOMs and only a few cells were fluorescent for the tracer infiltrated into the cerebellum. These latter labelings were present bilaterally, and their number and distribution did not show apparent differences after injecting the paramedian lobule and the vermal folia or the fastigial nucleus. Along the rostrocaudal extent of the oculomotor and trochlear nuclei, the neurons projecting to the cerebellum were intermingled with the motor neurons located in the nuclear area facing the medial longitudinal fasciculus. In the abducens nucleus they were restricted to the caudal pole of the nucleus, which is located ventrolaterally to the genu of the facial nerve. Double-labeled neurons were never found. The absence of double-labeled cells, in spite of the efficiency of the tracer infiltration into the EOMs and into the cerebellum, demonstrates that the cerebellar projections from the extraocular motor nuclei are not collaterals of the motor neurons, but axons of a separate population of neurons. (+info)
Role of the Botzinger complex in fastigial nucleus-mediated respiratory responses. (2/323)We have reported that the phrenic neurogram (PN) is modulated by stimulation of the fastigial nucleus (FN) of the cerebellum. The present study was undertaken to search for brainstem site(s) involved in the FN efferent pathway to modulate phrenic nerve activities. Experiments were performed on 35 anesthetized, paralyzed, and ventilated cats, using the PN as the index of the respiratory motor output. Results showed that bilateral electrolytic lesions of the red nucleus (RN), the paramedian reticular nucleus (PRN), or the pontine respiratory group (PRG) had little effect on the ability of FN stimulation to modulate the respiratory output. However, the modulation was abolished by bilateral electrolytic lesions of the Botzinger complex (BotC). Further studies showed that bilateral chemical inactivation of BotC neurons produced by topical microinjection of kainic acid or cobalt chloride failed to abolish the modulation. We concluded that fibers of passage, not synapses or cell bodies in the BotC, were involved in the modulatory effect of FN stimulation on the PN. The RN, PRN, and PRG appear not to be important in the neural circuitry responsible for the FN modulation of the phrenic activity. (+info)
Perineuronal nets of proteoglycans in the adult mouse brain, with special reference to their reactions to Gomori's ammoniacal silver and Ehrlich's methylene blue. (3/323)As our previous studies have indicated, many subsets of neurons in the vertebrate brain possess a sulfated proteoglycan surface coat which reacts to cationic iron colloid and aldehyde fuchsin. The present study demonstrated that this surface coat is supravitally stained with Ehrlich's methylene blue, and doubly with this blue and aldehyde fuchsin, a finding suggesting its being identical to Cajal's superficial reticulum (red superficial) and to Golgi's reticular coating (revetement reticulare). The perineuronal surface coat was further stained with Gomori's ammoniacal silver, and doubly with this silver and cationic iron colloid. These neurons with such a proteoglycan surface coat usually expressed cell surface glycoproteins which were labeled with lectin Wisteria floribunda agglutinin. Hyaluronidase digestion did not interfere with this lectin labeling of the glycoproteins, methylene blue and Gomori's ammoniacal silver staining of the surface coat, while it erased the cationic iron colloid and aldehyde fuchsin staining of the surface coat. These findings suggest that the perineuronal proteoglycan surface coat is associated with some additional molecules which are resistant to hyaluronidase digestion and stainable with methylene blue and Gomori's ammoniacal silver. The possibility is suggested that these molecules might represent "ligand proteoglycans" connecting the perineuronal proteoglycans and cell surface glycoproteins. (+info)
Intrinsic neurons of fastigial nucleus mediate neurogenic neuroprotection against excitotoxic and ischemic neuronal injury in rat. (4/323)Electrical stimulation of the cerebellar fastigial nucleus (FN) elevates regional cerebral blood flow (rCBF) and arterial pressure (AP) and provides long-lasting protection against focal and global ischemic infarctions. We investigated which neuronal element in FN, perikarya or axons, mediates this central neurogenic neuroprotection and whether it also protects against excitotoxicity. In anesthetized rats, the FN was stimulated for 1 hr, and ibotenic acid (IBO) was microinjected unilaterally into the striatum. In unstimulated controls, the excitotoxic lesions averaged approximately 40 mm3. Stimulation of FN, but not dentate nucleus (DN), significantly reduced lesion volumes up to 80% when IBO was injected 15 min, 72 hr, or 10 d, but not 30 d, thereafter. In other rats, intrinsic neurons of FN or DN were destroyed by pretreatment with IBO. Five days later, the FN was stimulated, and 72 hr later, IBO was microinjected into the striatum. Lesions of FN, but not DN, abolished neuroprotection but not the elevations of rCBF and AP elicited from FN stimulation. Excitotoxic lesions of FN, but not DN, also abolished the 37% reduction in focal ischemic infarctions produced by middle cerebral artery occlusion. Excitation of intrinsic FN neurons provides long-lasting, substantial, and reversible protection of central neurons from excitotoxicity, as well as focal ischemia, whereas axons in the nucleus, probably collaterals of ramified brainstem neurons, mediate the elevations in rCBF, which do not contribute to neuroprotection. Long-lived protection against a range of injuries is an unrecognized function of FN neurons transmitted over pathways distinct from those regulating rCBF. (+info)
Fastigial nucleus activity during different frequencies and orientations of vertical vestibular stimulation in the monkey. (5/323)Neurons in the rostral part of the fastigial nucleus (FN) respond to vestibular stimulation but are not related to eye movements. To understand the precise role of these vestibular-only neurons in the central processing of vestibular signals, unit activity in the FN of alert monkeys (Macaca mulatta) was recorded. To induce vestibular stimulation, the monkey was rotated sinusoidally around an earth-fixed horizontal axis at stimulus frequencies between 0.06 (+/-15 degrees) and 1.4 Hz (+/-7.5 degrees). During stimulation head orientation was changed continuously, allowing for roll, pitch, and intermediate planes of orientation. At a frequency of 0.6 Hz, 59% of the neurons had an optimal response orientation (ORO) and a null response (i.e., no modulation) 90 degrees apart. The phase of neuronal response was constant except for a steep shift of 180 degrees around the null response. This group I response is compatible with a semicircular canal input, canal convergence, or a single otolith input. Several other features indicated more complex responses, including spatiotemporal convergence (STC). 1) For 35% of the responses at 0.6 Hz, phase changes were gradual with different orientations. Fifteen percent of these had a null response (group II), and 20% showed only a minimal response but no null response (group III). The remaining responses (6%), classified as group IV, were characterized by a constant sensitivity at different orientations in most instances. 2) For the vast majority of neurons, the stimulus frequency determined the response group, i.e., an individual neuron could show a group I response at one frequency and a group II (III or IV) response at another frequency. 3) ORO changed with frequency by >45 degrees for 44% of the neurons. 4) Although phase changes at different frequencies were close to head velocity (+/-45 degrees ) or head position (+/-45 degrees ) for most neurons, they exceeded 90 degrees for 29% of the neurons between 0.1 and 1.0 Hz. In most cases, this was a phase advance. The change in sensitivity with change in frequency showed a similar pattern for all neurons; the average sensitivity increased from 1.24 imp. s-1. deg-1 at 0.1 Hz to 2.97 imp. s-1. deg-1 at 1.0 Hz. These data demonstrate that only an analysis based on measurements at different frequencies and orientations reveals a number of complex features. They moreover suggest that for the vast majority of neurons several sources of canal and otolith information interact at this central stage of vestibular information processing. (+info)
Simulations of cerebellar motor learning: computational analysis of plasticity at the mossy fiber to deep nucleus synapse. (6/323)We question the widely accepted assumption that a molecular mechanism for long-term expression of synaptic plasticity is sufficient to explain the persistence of memories. Instead, we show that learning and memory require that these cellular mechanisms be correctly integrated within the architecture of the neural circuit. To illustrate this general conclusion, our studies are based on the well characterized synaptic organization of the cerebellum and its relationship to a simple form of motor learning. Using computer simulations of cerebellar-mediated eyelid conditioning, we examine the ability of three forms of plasticity at mossy fiber synapses in the cerebellar nucleus to contribute to learning and memory storage. Results suggest that when the simulation is exposed to reasonable patterns of "background" cerebellar activity, only one of these three rules allows for the retention of memories. When plasticity at the mossy fiber synapse is controlled by nucleus or climbing fiber activity, the circuit is unable to retain memories because of interactions within the network that produce spontaneous drift of synaptic strength. In contrast, a plasticity rule controlled by the activity of the Purkinje cell allows for a memory trace that is resistant to ongoing activity in the circuit. These results suggest specific constraints for theories of cerebellar motor learning and have general implications regarding the mechanisms that may contribute to the persistence of memories. (+info)
Lateral cerebellar hemispheres actively support sensory acquisition and discrimination rather than motor control. (7/323)This study examined a new hypothesis proposing that the lateral cerebellum is not activated by motor control per se, as widely assumed, but is engaged during the acquisition and discrimination of tactile sensory information. This proposal derives from neurobiological studies of these regions of the rat cerebellum. Magnetic resonance imaging of the lateral cerebellar output nucleus (dentate) of humans during passive and active sensory tasks confirmed four a priori implications of this hypothesis. Dentate nuclei responded to cutaneous stimuli, even when there were no accompanying overt finger movements. Finger movements not associated with tactile sensory discrimination produced no dentate activation. Sensory discrimination with the fingers induced an increase in dentate activation, with or without finger movements. Finally, dentate activity was greatest when there was the most opportunity to modulate the acquisition of the sensory tactile data: when the discrimination involved the active repositioning of tactile sensory surface of the fingers. Furthermore, activity in cerebellar cortex was strongly correlated with observed dentate activity. This distinct four-way pattern of effects strongly challenges other cerebellar theories. However, contrary to appearances, neither our hypothesis nor findings conflict with behavioral effects of cerebellar damage, neurophysiological data on animals performing motor tasks, or cerebellar contribution to nonmotor, perceptual, and cognitive tasks. (+info)
Single-unit evidence for eye-blink conditioning in cerebellar cortex is altered, but not eliminated, by interpositus nucleus lesions. (8/323)Many theories of motor learning explain learning-related changes in motor behavior in terms of plasticity in the cerebellar cortex. Empirical evidence, however, does not always appear to be consistent with such formulations. It is the anterior cerebellar interpositus nucleus (aINP) that seems to be essential for acquisition and retention of conditioned eye-blink responses under most circumstances and it has been therefore suggested that the aINP is the critical site of learning-related plasticity during eye-blink conditioning. Supporting this conclusion are studies demonstrating that multiple-unit conditioning-related neural activity patterns observed in many brain regions disappear after aINP lesion. The possibility that the cerebellar cortex may be involved in forming these patterns has not been assessed adequately, however. In the current study, trained rabbits received kainic acid lesions of the INP. After recovery, the animals underwent additional sessions of conditioning during which single-unit activity was recorded from the cerebellar cortex. Our results suggest that the aINP is not the sole site of plasticity during eye-blink conditioning, as a subset of the neurons recorded from lesioned animals demonstrated conditioning-related firing patterns. The lesions did change the character of these firing patterns from those observed in saline controls, however, in ways that can be generally described as a loss of organization. The normal tendency for the population of cortical cells to change firing rate together, for instance, was significantly less noticeable in lesioned animals. These results suggest that the aINP may be involved in the production of important features of conditioned responding, such as system timing function, therefore suggesting the need for more models that incorporate aINP and brain stem feedback as integral to the production of organized neural and behavioral responses. (+info)
Some common types of cerebellar diseases include:
1. Cerebellar atrophy: This is a condition where the cerebellum shrinks or degenerates, leading to symptoms such as tremors, muscle weakness, and difficulty with movement.
2. Cerebellar degeneration: This is a condition where the cerebellum deteriorates over time, leading to symptoms such as loss of coordination, balance problems, and difficulties with speech and language.
3. Cerebellar tumors: These are abnormal growths that develop in the cerebellum, which can cause a variety of symptoms depending on their size and location.
4. Cerebellar stroke: This is a condition where blood flow to the cerebellum is interrupted, leading to damage to the brain tissue and symptoms such as weakness or paralysis of certain muscle groups.
5. Cerebellar vasculature disorders: These are conditions that affect the blood vessels in the cerebellum, leading to symptoms such as transient ischemic attacks (TIAs) or strokes.
6. Inflammatory diseases: These are conditions that cause inflammation in the cerebellum, leading to symptoms such as tremors, ataxia, and weakness.
7. Infections: Bacterial, viral, or fungal infections can affect the cerebellum and cause a range of symptoms.
8. Trauma: Head injuries or other forms of trauma can damage the cerebellum and lead to symptoms such as loss of coordination, balance problems, and memory loss.
9. Genetic disorders: Certain genetic mutations can affect the development and function of the cerebellum, leading to a range of symptoms.
10. Degenerative diseases: Conditions such as multiple sclerosis, Parkinson's disease, and Huntington's disease can cause degeneration of the cerebellum and lead to symptoms such as tremors, ataxia, and weakness.
It's important to note that this is not an exhaustive list, and there may be other causes of cerebellar symptoms not included here. A healthcare professional can help determine the underlying cause of your symptoms based on a thorough medical history and examination.
* Genetic mutations or deletions
* Infections such as meningitis or encephalitis
* Stroke or bleeding in the brain
* Traumatic head injury
* Multiple sclerosis or other demyelinating diseases
* Brain tumors
* Cerebellar degeneration due to aging
* Coordination difficulties, such as stumbling or poor balance
* Tremors or shaky movements
* Slurred speech and difficulty with fine motor skills
* Nystagmus (involuntary eye movements)
* Difficulty with gait and walking
* Fatigue, weakness, and muscle wasting
* Physical examination and medical history
* Neurological examination to test coordination, balance, and reflexes
* Imaging studies such as MRI or CT scans to rule out other conditions
* Genetic testing to identify inherited forms of cerebellar ataxia
* Electromyography (EMG) to test muscle activity and nerve function
* Physical therapy to improve balance, coordination, and gait
* Occupational therapy to help with daily activities and fine motor skills
* Speech therapy to address slurred speech and communication difficulties
* Medications to manage symptoms such as tremors or spasticity
* Assistive devices such as canes or walkers to improve mobility
* The prognosis for cerebellar ataxia varies depending on the underlying cause. In some cases, the condition may be slowly progressive and lead to significant disability over time. In other cases, the condition may remain stable or even improve with treatment.
Living with cerebellar ataxia can be challenging, but there are many resources available to help individuals with the condition manage their symptoms and maintain their quality of life. These resources may include:
* Physical therapy to improve balance and coordination
* Occupational therapy to assist with daily activities
* Speech therapy to address communication difficulties
* Assistive devices such as canes or walkers to improve mobility
* Medications to manage symptoms such as tremors or spasticity
* Support groups for individuals with cerebellar ataxia and their families
Overall, the key to managing cerebellar ataxia is early diagnosis and aggressive treatment. With proper management, individuals with this condition can lead active and fulfilling lives despite the challenges they face.
The symptoms of WE can vary depending on the severity of the deficiency, but common manifestations include:
1. Confusion and disorientation
2. Memory loss and difficulty learning new information
3. Difficulty with coordination and balance
4. Loss of muscle tone and weakness in the arms and legs
5. Disturbances in vision, hearing, and taste
6. Nausea and vomiting
7. Abnormalities in heart rate and blood pressure
8. Increased risk of seizures and coma
If left untreated, WE can lead to more severe complications such as Wernicke-Korsakoff Syndrome (WKS), a condition that involves the loss of brain tissue and memory loss. Treatment for WE typically involves thiamine supplements and addressing any underlying causes of the deficiency. In severe cases, hospitalization may be necessary to monitor and treat complications.
1. Fatigue and weakness: Thiamine is necessary for the production of ATP, the primary source of energy for the body's cells. Without enough thiamine, cells may not be able to produce enough ATP, leading to fatigue, weakness, and a lack of endurance.
2. Numbness and tingling: Thiamine is important for the health of the peripheral nerves, which can cause numbness, tingling, and pain in the hands and feet if there is a deficiency.
3. Memory loss and confusion: Thiamine is necessary for the proper functioning of the brain and can lead to memory loss, confusion, and difficulty concentrating if there is a deficiency.
4. Mood changes: Thiamine plays a role in the production of neurotransmitters, such as serotonin and dopamine, which are important for mood regulation. A thiamine deficiency can lead to mood changes, such as depression, anxiety, and irritability.
5. Digestive problems: Thiamine is necessary for the proper functioning of the digestive system, and a deficiency can lead to nausea, vomiting, diarrhea, and abdominal pain.
6. Heart problems: Thiamine is important for the health of the heart, and a deficiency can lead to heart failure, arrhythmias, and other cardiovascular problems.
7. Weight loss: Thiamine is necessary for the proper metabolism of carbohydrates, fats, and proteins, and a deficiency can lead to weight loss and muscle wasting.
8. Beriberi: A severe thiamine deficiency can lead to beriberi, a condition characterized by weakness, fatigue, and a range of other health problems.
Thiamine deficiency can be caused by a variety of factors, including:
1. Poor diet: A diet that is low in thiamine-rich foods, such as whole grains, lean meats, and fish, can lead to a deficiency.
2. Alcoholism: Alcohol can interfere with the absorption of thiamine in the gut, leading to a deficiency.
3. Gastrointestinal disorders: Certain conditions, such as Crohn's disease and ulcerative colitis, can lead to malabsorption of thiamine and other nutrients.
4. Medications: Some medications, such as furosemide and other diuretics, can interfere with the absorption of thiamine.
5. Genetic disorders: Certain genetic disorders, such as maple syrup urine disease, can lead to a thiamine deficiency.
If you suspect that you or someone you know may have a thiamine deficiency, it is important to consult with a healthcare professional for proper diagnosis and treatment. Treatment typically involves supplementation with thiamine, along with addressing any underlying causes of the deficiency. In severe cases, hospitalization may be necessary to manage symptoms and prevent complications.
The exact cause of thyroid crisis is not fully understood, but it is believed to be related to an autoimmune response that triggers the release of excessive amounts of thyroid hormones into the bloodstream. This can lead to a rapid increase in heart rate, cardiac arrhythmias, and other serious complications.
There are two main types of thyroid crisis:
1. Graves' disease-related thyroid crisis: This type is more common and typically affects people with Graves' disease, an autoimmune disorder that causes the thyroid gland to produce too much thyroxine (T4) and triiodothyronine (T3).
2. Toxic multinodular goiter-related thyroid crisis: This type is less common and occurs when multiple nodules in the thyroid gland produce excessive amounts of thyroid hormones.
The symptoms of thyroid crisis can vary depending on the severity of the condition, but they may include:
* Abdominal pain
* Heart palpitations
* Rapid heart rate
* Cardiac arrhythmias
* Shortness of breath
If you suspect that you or someone else is experiencing thyroid crisis, it is essential to seek medical attention immediately. Treatment typically involves hospitalization and may include the following:
1. Thyroid hormone-blocking medications: These drugs can help reduce the levels of thyroid hormones in the bloodstream and alleviate symptoms.
2. Antibiotics: If there are signs of infection, antibiotics may be prescribed to prevent or treat the infection.
3. Corticosteroids: These medications can help reduce inflammation in the thyroid gland and other parts of the body.
4. Cardiac support: In severe cases, cardiac support such as a pacemaker or defibrillator may be necessary to regulate the heart rhythm.
5. Surgery: In some cases, surgery may be required to remove part or all of the thyroid gland.
Preventing Thyroid Crisis
While there is no guaranteed way to prevent thyroid crisis, there are several measures you can take to reduce your risk:
1. Monitor your thyroid function: Regular blood tests can help identify any changes in thyroid hormone levels and allow for early treatment.
2. Manage underlying medical conditions: Conditions such as hypothyroidism, hyperthyroidism, and thyroid nodules can increase the risk of thyroid crisis. Proper management of these conditions can help reduce the risk.
3. Avoid stimulating the thyroid gland: Avoiding activities that stimulate the thyroid gland, such as strenuous exercise or excessive iodine intake, can help reduce the risk of thyroid crisis.
4. Seek prompt medical attention: If you experience any symptoms of thyroid crisis, seek prompt medical attention. Early treatment can help prevent complications and improve outcomes.
5. Be aware of your medications: Certain medications, such as steroids and amiodarone, can increase the risk of thyroid crisis. Be aware of the potential risks and discuss any concerns with your healthcare provider.
Living with Thyroid Crisis
Living with thyroid crisis can be challenging, but there are several resources and support options available to help you manage the condition:
1. Healthcare team: Your healthcare provider is your primary source of information and support. They can provide guidance on managing the condition and address any questions or concerns you may have.
2. Online resources: There are several online resources and support groups available for people with thyroid crisis, such as the American Thyroid Association and the Thyroid Foundation of America. These organizations provide information, resources, and support for people with thyroid conditions.
3. Support groups: Joining a support group can provide a sense of community and help you connect with others who are going through similar experiences.
4. Self-care: Engaging in self-care activities such as exercise, meditation, and relaxation techniques can help manage stress and improve overall well-being.
5. Advocating for yourself: Learning to advocate for yourself and your health is essential when living with thyroid crisis. Be proactive and assertive when communicating with your healthcare provider and loved ones about your needs and concerns.
Thyroid crisis, also known as thyroid storm or thyrotoxic crisis, is a life-threatening condition that requires prompt medical attention. It occurs when the thyroid gland becomes overactive and releases excessive amounts of thyroid hormones into the bloodstream. This can lead to symptoms such as fever, rapid heart rate, and muscle weakness.
If you suspect you or someone you know is experiencing a thyroid crisis, it is essential to seek medical attention immediately. Early treatment can help prevent complications and improve outcomes. Living with thyroid crisis can be challenging, but there are several resources and support options available to help manage the condition. By being proactive and advocating for yourself, you can improve your quality of life and manage this condition effectively.
There are several types of ophthalmoplegia, including:
1. External ophthalmoplegia: This type affects the muscles that control lateral and vertical movements of the eyes.
2. Internal ophthalmoplegia: This type affects the muscles that control rotational movements of the eyes.
3. Superior oblique paresis: This type affects the superior oblique muscle, which controls downward and outward movements of the eye.
4. Inferior oblique paresis: This type affects the inferior oblique muscle, which controls upward and outward movements of the eye.
Symptoms of ophthalmoplegia may include difficulty moving the eyes, double vision, droopy eyelids, and blurred vision. Treatment options depend on the underlying cause of the condition and may include physical therapy, prism lenses, or surgery.
The key symptoms of Korsakoff syndrome are:
* Memory loss: Sufferers experience difficulty in forming new memories, which can result in short-term memory loss. They may not remember recent events or conversations, and may have trouble recalling information they learned recently.
* Confabulation: Individuals with Korsakoff syndrome may fill in memory gaps with fabricated information, leading to confabulation (false memories). This can result in inaccurate or distorted recollections of past events.
* Dissociation: The condition can lead to dissociative symptoms such as depersonalization (feeling detached from oneself) and derealization (feeling detached from the world around them).
Korsakoff syndrome is a serious condition that requires prompt medical attention, particularly if it is caused by severe alcoholism or malnutrition. Treatment typically involves addressing the underlying cause of the disorder, such as stopping alcohol consumption and correcting any nutritional deficiencies. In some cases, medication may be prescribed to manage symptoms like anxiety or depression.
The condition is often seen in people who have a history of chronic alcoholism, although it can also occur in individuals with other conditions that affect the brain and central nervous system. Korsakoff syndrome can significantly impact an individual's ability to function in daily life, particularly if left untreated.
This condition is most commonly seen in people with advanced liver disease, such as cirrhosis or liver cancer. It can also be caused by other conditions that affect the liver, such as hepatitis or portal hypertension.
Symptoms of hepatic encephalopathy can include confusion, disorientation, slurred speech, memory loss, and difficulty with coordination and balance. In severe cases, it can lead to coma or even death.
Diagnosis of hepatic encephalopathy is typically made through a combination of physical examination, medical history, and diagnostic tests such as blood tests and imaging studies. Treatment options include medications to reduce the production of ammonia in the gut, antibiotics to treat any underlying infections, and transjugular intrahepatic portosystemic shunt (TIPS) to improve liver function. In severe cases, a liver transplant may be necessary.
Overall, hepatic encephalopathy is a serious condition that can have significant impact on quality of life and survival in people with advanced liver disease. Early detection and prompt treatment are essential to prevent complications and improve outcomes.
There are several types of intestinal obstruction, including:
1. Mechanical bowel obstruction: This type of obstruction is caused by a physical blockage in the intestine, such as adhesions or hernias.
2. Non-mechanical bowel obstruction: This type of obstruction is caused by a decrease in the diameter of the intestine, such as from inflammation or scarring.
3. Paralytic ileus: This type of obstruction is caused by a delay in the movement of food through the intestine, usually due to nerve damage or medication side effects.
4. Intestinal ischemia: This type of obstruction is caused by a decrease in blood flow to the intestine, which can lead to tissue damage and death.
Intestinal obstructions can be diagnosed through a variety of tests, including:
1. Abdominal X-rays: These can help identify any physical blockages in the intestine.
2. CT scans: These can provide more detailed images of the intestine and help identify any blockages or other issues.
3. Endoscopy: This involves inserting a flexible tube with a camera into the mouth and down into the intestine to visualize the inside of the intestine.
4. Biopsy: This involves removing a small sample of tissue from the intestine for examination under a microscope.
Treatment for intestinal obstructions depends on the underlying cause and severity of the blockage. Some common treatments include:
1. Fluid and electrolyte replacement: This can help restore hydration and electrolyte balance in the body.
2. Nasojejunal tube placement: A small tube may be inserted through the nose and into the jejunum to allow fluids and medications to pass through the blockage.
3. Surgery: In some cases, surgery may be necessary to remove the blockage or repair any damage to the intestine.
4. Medication: Depending on the underlying cause of the obstruction, medications such as antibiotics or anti-inflammatory drugs may be prescribed to help resolve the issue.
Preventing intestinal obstructions is often challenging, but some strategies can help reduce the risk. These include:
1. Avoiding foods that can cause blockages, such as nuts or seeds.
2. Eating a balanced diet and avoiding constipation.
3. Drinking plenty of fluids to stay hydrated.
4. Managing underlying medical conditions, such as inflammatory bowel disease or diabetes.
5. Avoiding medications that can cause constipation or other digestive problems.
Cecal neoplasms refer to abnormal growths or tumors that occur in the cecum, which is a part of the large intestine. The cecum is a pouch-like structure located at the junction of the small and large intestines. Cecal neoplasms can be benign (non-cancerous) or malignant (cancerous).
Types of Cecal Neoplasms
There are several types of cecal neoplasms, including:
1. Adenoma: A benign tumor that arises from the glandular cells lining the cecum.
2. Villous adenoma: A type of adenoma that is characterized by the growth of villi, which are finger-like projections of epithelial tissue.
3. Tubulovillous adenoma: A type of adenoma that is characterized by the growth of tubular and villous structures.
4. Mucinous cystic neoplasm: A benign tumor that arises from the mucin-secreting cells lining the cecum.
5. Intraepithelial neoplasms: Precancerous changes that occur in the epithelial cells lining the cecum.
6. Carcinoma: A malignant tumor that arises from the epithelial cells lining the cecum.
7. Squamous cell carcinoma: A type of carcinoma that is characterized by the growth of squamous cells.
8. Adenocarcinoma: A type of carcinoma that is characterized by the growth of glandular cells.
Causes and Risk Factors
The exact causes of cecal neoplasms are not known, but several risk factors have been identified, including:
1. Age: The risk of developing cecal neoplasms increases with age.
2. Family history: Having a family history of colon cancer or other gastrointestinal cancers increases the risk of developing cecal neoplasms.
3. Inflammatory bowel disease: People with inflammatory bowel diseases, such as ulcerative colitis and Crohn's disease, are at higher risk of developing cecal neoplasms.
4. Genetic mutations: Some genetic mutations, such as those associated with familial adenomatous polyposis (FAP) and Lynch syndrome, increase the risk of developing cecal neoplasms.
5. Diet and lifestyle factors: A diet high in processed meat and low in fiber may increase the risk of developing cecal neoplasms.
Cecal neoplasms may not cause any symptoms in the early stages, but as they grow, they can cause a variety of symptoms, including:
1. Abdominal pain or discomfort
2. Changes in bowel movements (such as diarrhea or constipation)
3. Blood in the stool
4. Weakness and fatigue
5. Loss of appetite
6. Unexplained weight loss
The diagnosis of cecal neoplasms is based on a combination of clinical findings, imaging studies, and pathological examination of tissue samples. The following tests may be used to diagnose cecal neoplasms:
1. Endoscopy: A flexible tube with a camera and light on the end is inserted through the mouth or rectum to visualize the inside of the cecum and collect tissue samples.
2. Imaging studies: Computed tomography (CT) scans, magnetic resonance imaging (MRI), or positron emission tomography (PET) scans may be used to identify any abnormalities in the cecum and surrounding tissues.
3. Biopsy: A sample of tissue is taken from the cecum during endoscopy or surgery and examined under a microscope for cancer cells.
4. Blood tests: Blood tests may be used to check for certain substances in the blood that are associated with cancer, such as carcinoembryonic antigen (CEA).
The treatment of cecal neoplasms depends on the type and stage of the cancer. The following options may be considered:
1. Surgery: Surgical removal of the cancerous tissue may be recommended for early-stage cancers.
2. Chemotherapy: Chemotherapy may be used in combination with surgery or as a standalone treatment for more advanced cancers.
3. Radiation therapy: Radiation therapy may be used in combination with chemotherapy or surgery to treat cancer that has spread to other parts of the body.
4. Targeted therapy: Targeted therapy may be used to treat specific genetic mutations that are driving the growth of the cancer.
The prognosis for cecal neoplasms depends on the type and stage of the cancer at the time of diagnosis. In general, early-stage cancers have a better prognosis than more advanced cancers. Factors that may affect prognosis include:
1. Type of cancer: The type of cancer present in the cecum can impact prognosis. For example, adenocarcinoma has a better prognosis than squamous cell carcinoma.
2. Stage of cancer: Cancers that have spread to other parts of the body (metastasized) have a poorer prognosis than those that are localized to the cecum.
3. Age and overall health: Older patients or those with underlying health conditions may have a poorer prognosis than younger, healthier individuals.
4. Treatment options: The effectiveness of treatment can also impact prognosis. Patients who receive early and appropriate treatment may have a better prognosis than those who do not receive timely treatment.
The survival rate for cecal neoplasms is generally lower than for other types of gastrointestinal cancers. According to the American Cancer Society, the 5-year survival rate for cecal cancer is approximately 20%. This means that of patients diagnosed with cecal cancer, about 20% are still alive 5 years after their initial diagnosis. However, it's important to note that this is a general estimate and individual prognosis can vary based on a variety of factors.
There are several lifestyle changes that may help reduce the risk of developing cecal neoplasms or improve outcomes for those who have been diagnosed:
1. Maintain a healthy diet and weight: Eating a balanced diet high in fruits, vegetables, and whole grains can help reduce the risk of developing cecal cancer. Additionally, maintaining a healthy weight can help reduce the risk of developing many types of cancer.
2. Exercise regularly: Regular physical activity has been shown to reduce the risk of developing many types of cancer, including cecal cancer.
3. Avoid tobacco and excessive alcohol consumption: Tobacco use and excessive alcohol consumption have both been linked to an increased risk of developing cecal cancer. Quitting smoking and limiting alcohol intake can help reduce the risk of developing this disease.
4. Manage chronic conditions: Chronic conditions such as diabetes, obesity, and inflammatory bowel disease can increase the risk of developing cecal cancer. Managing these conditions through lifestyle changes and medication can help reduce the risk of developing this disease.
5. Get regular screenings: Regular screenings for colon cancer, such as colonoscopies, can help detect cecal cancer at an early stage when it is more treatable.
6. Consider aspirin therapy: Some studies have suggested that taking a low-dose aspirin every day may help reduce the risk of developing colorectal cancer, including cecal cancer. However, aspirin therapy is not right for everyone, and individuals should talk to their doctor before starting any new medication.
7. Don't delay symptoms: If you experience any symptoms that may be related to cecal cancer, such as abdominal pain or changes in bowel movements, don't delay seeking medical attention. These symptoms can also be caused by other conditions, but it is important to get them checked out by a healthcare professional.
It is important to note that these recommendations are not a guarantee against developing cecal cancer, and individuals should talk to their doctor about their specific risk factors and any additional steps they can take to reduce their risk of developing this disease.
1. Ulcerative colitis: This is a chronic condition that causes inflammation and ulcers in the colon. Symptoms can include abdominal pain, diarrhea, and rectal bleeding.
2. Crohn's disease: This is a chronic condition that affects the digestive tract, including the colon. Symptoms can include abdominal pain, diarrhea, fatigue, and weight loss.
3. Irritable bowel syndrome (IBS): This is a common condition characterized by recurring abdominal pain, bloating, and changes in bowel movements.
4. Diverticulitis: This is a condition where small pouches form in the colon and become inflamed. Symptoms can include fever, abdominal pain, and changes in bowel movements.
5. Colon cancer: This is a type of cancer that affects the colon. Symptoms can include blood in the stool, changes in bowel movements, and abdominal pain.
6. Inflammatory bowel disease (IBD): This is a group of chronic conditions that cause inflammation in the digestive tract, including the colon. Symptoms can include abdominal pain, diarrhea, fatigue, and weight loss.
7. Rectal cancer: This is a type of cancer that affects the rectum, which is the final portion of the colon. Symptoms can include blood in the stool, changes in bowel movements, and abdominal pain.
8. Anal fissures: These are small tears in the skin around the anus that can cause pain and bleeding.
9. Rectal prolapse: This is a condition where the rectum protrudes through the anus. Symptoms can include rectal bleeding, pain during bowel movements, and a feeling of fullness or pressure in the rectal area.
10. Hemorrhoids: These are swollen veins in the rectum or anus that can cause pain, itching, and bleeding.
It's important to note that some of these conditions can be caused by other factors as well, so if you're experiencing any of these symptoms, it's important to see a doctor for an accurate diagnosis and treatment.
Deep cerebellar nuclei
Arbor vitae (anatomy)
Succinic semialdehyde dehydrogenase deficiency
Cerebellar cognitive affective syndrome
White matter dissection
Spinocerebellar ataxia type 1
Mossy fiber (cerebellum)
Multiple system atrophy
R-type calcium channel
Posterior lobe of cerebellum
Medial medullary syndrome
Medial vestibular nucleus
Short-term effects of alcohol consumption
Primate basal ganglia
Radial glial cell
Neuronal cell cycle
Multiple sclerosis signs and symptoms
Index of anatomy articles
Hereditary dentatorubral-pallidoluysian atrophy: ubiquitinated filamentous inclusions in the cerebellar dentate nucleus neurons...
ModelDB: Robust transmission in the inhibitory Purkinje Cell to Cerebellar Nuclei pathway (Abbasi et al 2017)
Histamine improves rat rota-rod and balance beam performances through H(2) receptors in the cerebellar interpositus nucleus. |...
Parrots have evolved a primate-like telencephalic-midbrain-cerebellar circuit | Scientific Reports
Topographic distribution of output neurons in cerebellar nuclei and cortex to somatotopic map of primary motor cortex
Loss of deep cerebellar nuclei neurons in the 3xTg-AD mice and protection by an anti-amyloid β antibody fragment | AlzPED
Schwarz Lab : Hertie-Institut für klinische Hirnforschung
Contribution of cerebral edema to the neuronal salvage elicited by stimulation of cerebellar fastigial nucleus after occlusion...
Frontiers | A Biomimetic Control Method Increases the Adaptability of a Humanoid Robot Acting in a Dynamic Environment
Intrinsic Plasticity of Cerebellar Purkinje Cells Contributes to Motor Memory Consolidation | Journal of Neuroscience
Tissue expression of FARP2 - Staining in cerebellum - The Human Protein Atlas
A multimodal cell census and atlas of the mammalian primary motor cortex - PubMed
MESH TREE NUMBER CHANGES - 2008 MeSH
Joubert syndrome: brain and spinal cord malformations in genotyped cases and implications for neurodevelopmental functions of...
Cockayne syndrome - About the Disease - Genetic and Rare Diseases Information Center
Addgene: pAAV-hSyn-hChR2(H134R)-EYFP Citations
Early Childhood Neurobehavioral Assessment for the Differential Diagnosis of Fetal Alcohol Syndrome and Alcohol-Related...
Úloha centrálneho nervového systému v etiopatogené... | proLékaře.cz
Portal Regional da BVS
Why you feel full after eating | National Institutes of Health (NIH)
Jing Huang - NeL.edu
TREE NUMBER DESCRIPTOR
Santiago Ramón y Cajal Exhibit - Office of NIH History and Stetten Museum
Incremento del glutamato en el estriado de asociación en esquizofrenia. Resultados preliminares de un estudio longitudinal con...
- Motor and non-motor territories of the human dentate nucleus: Mapping the topographical connectivity of the cerebellar cortex with in-vivo sub-millimeter diffusion imaging. (mpg.de)
- Ultrastructural lesions in the caudate nucleus and cerebellar cortex. (bvsalud.org)
- The cerebellar cortex is a principal receiver of M1 projections via pons, but the emergent dynamics in these regions with motor skill learning is incompletely understood. (eneuro.org)
- Pathologically the cerebellar cortex and subcortical nuclei demonstrate diffuse degenerative changes. (uchicago.edu)
- Infantile neuroaxonal dystrophy Cerebellar atrophy(95%) T2 hypointensity in Gp,SN(50%) Spares cortex Neuroferitinopathy T2 hypointensity in GP, SN Then dendate /caudate nuclei,thalami Affects cortex Aceruloplasminemia. (barnard.in)
- It is also known as the "little brain" with convolutions similar to those of CEREBRAL CORTEX, inner white matter, and deep cerebellar nuclei. (uams.edu)
- Here, we examined the effects of WF on the frontal cortex (FCT, including pre-frontal cortex), parietal cortex (PCT, including motor cortex), and thalamus (THL, including subthalamic nucleus) of rats to determine if it instigates neurochemical and synaptic changes that are predictive of sensorimotor and cognitive impairment. (cdc.gov)
- Furthermore, the observed defects in the intrinsic plasticity of PCs led to the formation of aberrant neural plasticity in the vestibular nucleus neurons. (jneurosci.org)
- As a PhD student in Johns Hopkins with David Linden, I studied plasticity of inhibitory inputs and of intrinsic excitability of deep-cerebellar nuclear neurons. (brown.edu)
- Four clusters of neurons located deep within the WHITE MATTER of the CEREBELLUM, which are the nucleus dentatus, nucleus emboliformis, nucleus globosus, and nucleus fastigii. (bvsalud.org)
- Discharge of identified deep cerebellar nuclei neurons related to eye blinks in the alert cat. (bvsalud.org)
- To explore the pathogenesis of migraine chronification, we measured gamma-aminobutyric acid (GABA) and glutamate/glutamine (Glx) levels in the dentate nucleus (DN) and PAG of patients with episodic and chronic migraine and healthy subjects. (biomedcentral.com)
- MRI brain revealed symmetric hyperintense lesions in the dentate nucleus and pons on T2-weighted imaging and FLAIR, which have a well-established association with metronidazole-induced central nervous system (CNS) toxicity. (who.int)
- Both teams aimed at the same target, the ventralis intermedius nucleus of the thalamus (VIM), but team A found a clear improvement of choreic peak dose dyskinesias, whereas team B did not consistently. (bmj.com)
- Essential tremor can be suppressed with chronic, bilateral deep brain stimulation (DBS) of the ventralis intermedius nucleus (Vim), the cerebellar receiving area of the motor thalamus. (northwestern.edu)
- In the case of primates, increasing evidence suggests that the cerebellum and cortico-cerebellar pathways play an essential role in complex cognitive abilities like the ones mentioned above 10 , 11 . (nature.com)
- Here, we report on low-frequency oscillatory (LFO) activity that emerges in cortico-cerebellar networks with learning the reach-to-grasp motor skill. (eneuro.org)
- This work furthers our understanding on emergent dynamics in the cortico-cerebellar loop that underlie learning and execution of precise skilled movement. (eneuro.org)
- Recent interest in modulating cortico-cerebellar networks for motor recovery postinjury/stroke make this work an important precursor to assessing whether similar low-frequency activity in cortico-cerebellar networks can serve as a biomarker of motor recovery and help to optimize the modulation of these networks. (eneuro.org)
- but similar oscillatory dynamics have not been studied in cortico-cerebellar networks. (eneuro.org)
- In mammals, the evolution of complex cognitive abilities is associated with increases in the size of the telencephalon and cerebellum as well as the pontine nuclei, which connect these two regions. (nature.com)
- Like mammals, birds have two brainstem pontine nuclei that project to the cerebellum and receive projections from the telencephalon. (nature.com)
- Unlike mammals, birds also have a pretectal nucleus that connects the telencephalon with the cerebellum: the medial spiriform nucleus (SpM). (nature.com)
- Dopamine-glutamate reciprocal modulation of release and motor responses in the rat caudate-putamen and nucleus accumbens of intact animals. (medigraphic.com)
- Although plasticity of excitability, intrinsic plasticity, of the cerebellar Purkinje cell has been reported in both directions (potentiation and depression), the physiological role of intrinsic plasticity still remains ambiguous. (jneurosci.org)
- Our results suggest that intrinsic plasticity of cerebellar Purkinje cell has a significant role in motor memory consolidation. (jneurosci.org)
- Cuatro acúmulos de neuronas, de localización profunda, en la SUSTANCIA BLANCA del CEREBELO, que reciben los nombres de núcleo dentado, núcleo emboliforme, núcleo globoso y núcleo medial o fastigio. (bvsalud.org)
- Deep brain stimulation (DBS) has become a widely accepted method for the treatment of Parkinson's disease symptoms and concerns three major targets-namely, the nucleus ventralis intermedius (VIM), the internal part of the globus pallidus (GPi), and the subthalamic nucleus (STN). (bmj.com)
- these cells are particularly affected by expansion of the gene, leading to cerebellar atrophy. (medlineplus.gov)
- MRI brain: Bilateral symmetric areas of gradient blooming noted in susceptibility weighted images in lentiform nucleus( globus pallidus) It is noted in T2 and FLAIR sequences as well. (barnard.in)
- This suggests that the telencephalon-SpM-cerebellar pathway of birds may play an analogous role to cortico-ponto-cerebellar pathways of mammals in controlling fine motor skills and complex cognitive processes. (nature.com)
- We chronically recorded the motor and the cerebellar cortices in rats, which revealed the emergence of coordinated movement-related activity in the local-field potentials as the reaching skill consolidated. (eneuro.org)
- Elsawy H, Alzahrani AM, Alfwuaires M, Sedky A, El-Trass EE, Mahmoud O, Abdel-Moneim AM, Khalil M. Analysis of silymarin-modulating effects against acrylamide-induced cerebellar damage in male rats: Biochemical and pathological markers. (uams.edu)
- Our results suggest that synergistic modulation of intrinsic and synaptic plasticity in PCs is required for the changes in downstream plasticity in the vestibular nucleus, and thereby contributing to the long-term storage of motor memory. (jneurosci.org)
- In this study, we suggest that both synaptic and intrinsic plasticity are required for successful memory consolidation in cerebellar eye movement learning. (jneurosci.org)
- Here, we provide insight into the circuit mechanism through which intrinsic plasticity of cerebellar PCs may be required for long-term memory storage. (jneurosci.org)
- 2 . Steuber V, Schultheiss NW, Silver RA, De Schutter E, Jaeger D (2011) Determinants of synaptic integration and heterogeneity in rebound firing explored with data-driven models of deep cerebellar nucleus cells. (yale.edu)
- Pathological findings of anti-Yo cerebellar degeneration with Holmes tremor. (uchicago.edu)
- Paraneoplastic Cerebellar Degeneration" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (uchicago.edu)
- Spatiotemporal changes in along-tract profilometry of cerebellar peduncles in cerebellar mutism syndrome. (uams.edu)
- In VOR circuits, cerebellar PCs integrate the information and then project their output signal to the VN. (jneurosci.org)
- Together, our findings support the notion that a complex interplay of overlapping neural circuits, primarily involving nigrostriatal, cortical, thalamic, and cerebellar tracts are critical for eliciting key motor and non-motor symptoms in PD, and perhaps manganism, as well as welding -mediated PD-like manifestation. (cdc.gov)
- Cerebellar Transcriptomic Analysis in a Chronic plus Binge Mouse Model of Alcohol Use Disorder Demonstrates Ethanol-Induced Neuroinflammation and Altered Glial Gene Expression. (uams.edu)
- Divergent and overlapping hippocampal and cerebellar transcriptome responses following developmental ethanol exposure during the secondary neurogenic period. (uams.edu)
- Auditory hallucinations across the psychosis spectrum: Evidence of dysconnectivity involving cerebellar and temporal lobe regions. (uams.edu)
- We found that SpM, but not the pontine nuclei, is greatly enlarged in parrots and its relative size significantly correlated with the relative size of the telencephalon across all birds. (nature.com)
- 3 . Steuber V, Jaeger D (2013) Modeling the generation of output by the cerebellar nuclei. (yale.edu)
- This graph shows the total number of publications written about "Paraneoplastic Cerebellar Degeneration" by people in this website by year, and whether "Paraneoplastic Cerebellar Degeneration" was a major or minor topic of these publications. (uchicago.edu)
- We conclude that SpM is key to understanding the role of telencephalon-cerebellar pathways in the evolution of complex cognitive abilities in birds. (nature.com)