Amnesia, Transient Global
Alcohol Amnestic Disorder
Ischemic Attack, Transient
Autobiography as Topic
Magnetic Resonance Imaging
Brain Damage, Chronic
Anterior Thalamic Nuclei
Multiple Personality Disorder
Androgen Receptor Antagonists
Prostatic Neoplasms, Castration-Resistant
NF-kappa B p52 Subunit
Lack of evidence of acute ischemic tissue change in transient global amnesia on single-shot echo-planar diffusion-weighted MRI. (1/30)BACKGROUND AND PURPOSE: There is uncertainty concerning the etiology of transient global amnesia (TGA). Previous CT and MRI studies have indicated that permanent structural abnormality is rare in TGA. Diffusion-weighted (DW) MRI is very sensitive to early ischemic parenchymal changes and has recently demonstrated embolic infarction in the posterior cerebral artery territory in 2 TGA patients. We report the findings of DW MRI in 8 patients in acute stages of TGA. METHODS: Conventional and echo-planar DW MRI was performed in 2 patients in the active phase and 6 patients in the recovery phase (1 to 8 hours after cessation of anterograde memory dysfunction) of spontaneously occurring TGA. RESULTS: None of the patients showed signs of hyperintensity on DW images or hypointensity on quantitative apparent diffusion coefficient (ADC) maps to suggest regional decreases of water mobility or acute T2 changes on transverse or coronal slices. CONCLUSIONS: We were unable to detect ADC or acute T2 changes with echo-planar DW MRI in patients with TGA, which suggests that mechanisms other than ischemic infarction may cause TGA. We did not identify spreading depression-associated changes of the ADC. Further refinement of MRI sequences may be necessary to detect subtle or transient signal change in brain parenchyma. (+info)
Relationship between migraine and cardiac and pulmonary right-to-left shunts. (2/30)A relationship between migraine with aura and the presence of right-to-left shunts has been reported in two studies. Right-to-left shunts are also associated with some forms of decompression illness. While conducting research in divers with decompression illness, it was our impression that divers with a large shunt often had a history of migraine with aura in everyday life and after dives. Therefore we routinely asked all divers about migraine symptoms. The medical records of the last 200 individuals referred for investigation of decompression illness were reviewed to determine the association between right-to-left shunts and migraine aura after diving, and migraine in daily life unconnected with diving. Migraine with aura in daily life unconnected with diving occurred significantly more frequently in individuals who had a large shunt which was present at rest (38 of 80; 47.5%) compared with those who had a shunt which was smaller or only seen after a Valsalva manoeuvre (four of 40; 10%) or those with no shunt (11 of 80; 13.8%) (P<0.001). Hemiplegic migraine occurred in 10 divers, each of whom had a shunt that was present at rest; in eight of these cases the shunt was large. The prevalence of migraine without aura was similar in all groups. Post-dive migraine aura was significantly more frequent in individuals who had a large shunt present at rest (21 of 80; 26.3%) compared with those who had a shunt that was smaller or only seen after a Valsalva manoeuvre (five of 40; 12.5%) or no shunt (one of 80; 1.3%) (P<0.001). Thus individuals with a large right-to-left shunt have an increased prevalence of migraine with aura in daily life unconnected with diving, and they also have an increased incidence of migraine aura after dives, but only when the dives liberate venous bubbles. These data suggest the possibility that, in some individuals, right-to-left shunts have a role in the aetiology of migraine with aura. The observations suggest that paradoxical gas embolism may precipitate migraine with aura. (+info)
Contrast study on cognitive function with MRI and positron emission tomography imaging in transient global amnesia. (3/30)OBJECTIVE: To study cognitive function and cerebral metabolic changes in patients with transient global amnesia (TGA). METHODS: Three patients with TGA were given mini-mental state examination (MMSE), revised Wechsler memory scale (WMS-R) examination and magnetic resonance imaging (MRI) scans after they had been diagnosed as TGA. Using (18)F labelled deoxyglucose as tracer, patients were given a positron emission tomography (PET) examination at different periods during recovery. RESULTS: No obvious abnormality was found in MMSE and MRI scans in the three patients. However, WMS-R examination and cerebral PET imaging displayed cognitive dysfunction of varying degrees and low metabolism in local areas related to memory in 2 of 3 patients. CONCLUSIONS: In TGA patients, cognitive function and cerebral metabolic levels are closely correlated with duration of symptoms. It is necessary to stop the TGA attack as quickly as possible early time. (+info)
Working memory and executive functions in transient global amnesia. (4/30)Transient global amnesia (TGA) is usually considered to produce a profound impairment of long-term episodic memory, while at the same time sparing working memory. However, this neuropsychological dissociation has rarely been examined in detail. While a few studies have assessed some components of working memory in TGA, the results that have been obtained are far from conclusive. To clarify this issue, we carried out a comprehensive investigation of working memory in 10 patients during a TGA attack. In the first study, we report the results from three patients examined with a battery of neuropsychological tests designed to assess each of the three subcomponents of Baddeley's model of working memory. In a second study, seven different patients underwent neuropsychological investigations that focused specifically on the central executive system, using a protocol derived from a study by Miyake and colleagues. Our findings showed that subcomponents of working memory, such as the phonological loop and visuo-spatial sketch pad, were spared in TGA patients. Specific executive functions that entailed inhibitory control, dual task performance, updating and shifting mechanisms were also found to be normal. However, we found significantly impaired performance for the Brown-Peterson test, and that TGA patients were significantly impaired in the recollection of their episodic memories. They also made reduced numbers of 'remember' compared with 'know' judgments in the episodic memory test several days after TGA. On the basis of our findings, it would appear that the episodic memory deficit during TGA is not related to elementary aspects of executive functioning. Our data also highlight the nature of the cognitive mechanisms involved in the Brown-Peterson task, which may well depend on long-term memory (such as the process of semantic encoding). Lastly, the selective deficit in recollective episodic memories observed in TGA may be principally related to medial temporal lobe abnormalities that have been reported in this syndrome. (+info)
The dynamic time course of memory recovery in transient global amnesia. (5/30)AIMS: To investigate the dynamic time course of transient global amnesia (TGA)--that is, the process of recovery and the interindividual variability--by testing four patients during the day of TGA itself (on three occasions) and at follow up (on two occasions). METHODS: A specially designed protocol focusing on semantic (both conceptual and autobiographical knowledge) and episodic (both anterograde and retrograde components) memory. RESULTS: Every patient showed marked impairment of both anterograde and retrograde episodic memory during the acute phase, with a relative preservation of personal and conceptual semantic knowledge. During the following phase, the authors observed similarities and differences among the patients' patterns of recovery. In general, retrograde amnesia recovered before the anterograde amnesia and anterograde episodic memory was recovered gradually in every case. In contrast, shrinkage of retrograde amnesia was more heterogeneous. In two of the patients, this shrinkage followed a chronological gradient and the most remote events were recovered first. In the two other patients, it depended more on the strength of the trace, and there was no temporal gradient. For the latter, an executive deficit could account for difficulties in accessing both conceptual knowledge and autobiographical memories. CONCLUSIONS: This profile of recovery suggests a "neocortical to medial temporal" process in every case, and the possibility of an additional frontal dysfunction in some cases. Hence, the acute phase seems to be characterised by a common episodic impairment. This variability between subjects appears in the recovery phase with two different patterns of impairment. (+info)
Internal jugular vein valve incompetence and intracranial venous anatomy in transient global amnesia. (6/30)BACKGROUND: Recently a causal relation between internal jugular vein valve incompetence (IJVVI) and transient global amnesia (TGA) has been suggested. IJVVI is postulated to provoke a transient mesiotemporal ischaemia by venous congestion. This mechanism requires a patent venous pathway from the affected IJV through the transverse sinus, confluens, straight sinus (SS), vein of Galen into the basal vein of Rosenthal and the internal cerebral veins. OBJECTIVE: To study IJVVI in TGA patients in relation to the intracranial venous anatomy. METHODS: IJVVI was defined if a repeated Valsalva manoeuvre (VM) led to a retrograde jugular flow detected by extracranial duplex ultrasound. Non-contrast venous MR angiography (MRA) was performed to analyse intracranial drainage patterns of the SS in relation to the side of the IJVVI. SS drainage was differentiated into three groups: predominantly right, left, and bilateral drainage. Ultrasound studies were performed in 25 TGA patients and 85 age matched controls. Twenty patients underwent venous MRA. RESULTS: Sixty eight per cent of patients and 33% of controls showed unilateral or bilateral IJVVI (p = 0.0025). In 36% of patients a TGA preceding VM was reported. Drainage pattern of SS and side of IJVVI corresponded in five of eight patients (63%) with VM and four of 12 patients without VM (33%, p = 0.0994). CONCLUSION: Our study confirms the significantly higher prevalence of IJVVI in TGA patients. However, no specific IJVVI related intracranial venous drainage patterns could be found to further support the hypothesis of a direct causal relation between IJVVI and TGA. (+info)
What does transient global amnesia really mean? Review of the literature and thorough study of 142 cases. (7/30)Since the first reports of transient global amnesia (TGA) were published in 1956, several neuropsychological and functional imaging studies have shed light on different aspects of this neurological syndrome. By establishing diagnostic criteria, Hodges and Warlow (1990b) have made it far easier to identify clinical TGA-related features. However, no comprehensive survey has been yet carried out in order to validate their criteria/findings or provide information about previously unknown features. In the present paper, (i) we review the literature published since Hodges and Warlow's study and seek to characterize the demographic and clinical features of TGA more accurately, (ii) we report 142 personal TGA cases, with supplementary information regarding both episodes and patients, such as precipitating events, associated symptoms and personality, and (iii) we suggest the existence of different groups of TGA patients, on the basis of a hierarchical cluster analysis. This revealed that in women, episodes are mainly associated with an emotional precipitating event, a history of anxiety and a pathological personality. In men, they occur more frequently after a physical precipitating event. In younger patients, a history of headaches may constitute an important risk factor. No link was found with vascular risk factors. The relevance of each of the above-mentioned variables is discussed in the light of our classification. An extensive description of cases from both the literature and our patient population allows us to refine the characterization of clinical TGA features. (+info)
Selective affection of hippocampal CA-1 neurons in patients with transient global amnesia without long-term sequelae. (8/30)The aetiology, pathomechanisms and anatomical correlates of transient global amnesia (TGA) still remain obscure. Recently, focal MR-signal diffusion-weighted imaging (DWI) changes in the hippocampus have been described in patients with TGA, but the exact localization, long term outcome and pathophysiological nature of these lesions still remain unknown. The topography and time course of hippocampal DWI lesions in 41 TGA patients was studied using serial 3 T high-resolution MR-imaging and correlated to clinical and neuropsychometric results. Of these, 29 patients showed 36 DWI lesions with corresponding T(2) lesions in the hippocampus within a time window of 48 h after onset. Almost all lesions (94%; 34/36) were selectively found in the CA-1 sector (Sommer sector) of the hippocampal cornu ammonis. Most DWI lesions (8/10) were already detectable in the peri-acute phase <6 h after onset of symptoms. A follow-up study 4-6 months after the episode did not show evidence for residual structural sequelae of these lesions (n = 20/20). A venous MR angiography of the intracranial dural sinus showed an asymmetric venous drainage in 21/24 (88%) patients. In 11/16 (69%) patients with unilateral lesions, the asymmetry corresponded to the side of the DWI lesion. Significant episodic verbal memory deficits in the acute phase (n = 14/18) were associated with lesions of the dominant hemisphere while impairment of visuospatial memory was associated with lesions of the non-dominant hemisphere. Persistent neuropsychological sequelae were not detected 4-6 months after the episode (n = 16). This is the first prospective study combining high-resolution imaging and neuropsychometry analysing the detailed functional anatomy and outcome of hippocampal DWI/T(2) lesions in TGA supporting the view the TGA being a benign transient disorder. The TGA can be considered a model for a focal transient perturbation of memory circuits in the temporo-mesial region. (+info)
There are different types of amnesia, including:
1. Retrograde amnesia: loss of memory of events that occurred before the onset of amnesia.
2. Anterograde amnesia: inability to form new memories after the onset of amnesia.
3. Transient global amnesia: temporary and reversible loss of memory due to a specific cause, such as a stroke or a head injury.
4. Korsakoff's syndrome: a condition caused by alcoholism and malnutrition that affects the hippocampus and the ability to form new memories.
5. Dissociative amnesia: loss of memory due to psychological trauma or stress, often accompanied by dissociation from reality.
The symptoms of amnesia can vary depending on the underlying cause and the severity of the condition. Some common symptoms include:
1. Difficulty learning new information
2. Forgetting recent events or conversations
3. Inability to recall past events or experiences
4. Confusion and disorientation
5. Difficulty with problem-solving and decision-making
The diagnosis of amnesia is based on a combination of medical history, physical examination, and neuropsychological tests. Imaging studies such as CT or MRI scans may also be used to rule out other causes of memory loss.
Treatment for amnesia depends on the underlying cause and may include:
1. Medications to manage symptoms such as anxiety, depression, or cognitive impairment.
2. Cognitive rehabilitation therapy to improve memory and problem-solving skills.
3. Behavioral interventions to help the individual adapt to their condition.
4. In some cases, surgery may be necessary to treat the underlying cause of amnesia, such as a tumor or a blood clot.
Overall, amnesia can have a significant impact on an individual's quality of life, but with proper diagnosis and treatment, many people are able to manage their symptoms and lead fulfilling lives.
Retrograde amnesia can be caused by a variety of factors, including traumatic brain injury, stroke, infection, or degenerative diseases such as Alzheimer's disease. The exact cause of retrograde amnesia will depend on the underlying medical condition.
One well-known example of retrograde amnesia is the case of patient H.M., who underwent surgery to remove a severe epileptic focus in his brain in 1953. The surgery involved the removal of large portions of his medial temporal lobe, including the hippocampus and other structures critical for memory formation. As a result of the surgery, patient H.M. developed retrograde amnesia, unable to recall events that occurred before the surgery. However, he was able to form new memories after the surgery, leading researchers to study his case extensively and gain insights into the neural mechanisms of memory formation.
Retrograde amnesia can be diagnosed through a combination of medical history, physical examination, neuropsychological tests, and imaging studies such as CT or MRI scans. Treatment for retrograde amnesia will depend on the underlying cause, and may include medications, rehabilitation therapies, or other interventions aimed at improving memory function.
In summary, retrograde amnesia is a condition where an individual experiences memory loss for events that occurred before a specific point in time, usually as a result of brain injury or disease. The exact cause of retrograde amnesia will depend on the underlying medical condition, and diagnosis and treatment will be tailored to the individual case.
People with anterograde amnesia may be able to remember events and information from before the onset of the condition, but they are unable to retain new information or form new memories. This can make it difficult for them to learn new skills or adapt to new situations.
The term "anterograde" refers to the fact that the condition affects the ability to form new memories, and not the ability to recall past memories. In other words, the person's memories from before the onset of the condition are preserved, but they are unable to create new ones.
Anterograde amnesia is often seen in combination with retrograde amnesia, which is the loss of memories from a specific time period or event. Together, these two types of amnesia can result in significant memory impairment and difficulty adapting to new situations.
The exact cause of TGA is unknown, but it is believed to be related to a temporary disruption in the blood flow to the Temporal lobe of the brain, which is responsible for memory formation and retrieval. Some possible triggers include:
* Head injury or trauma
* Emotional stress or anxiety
* Physical exertion or overexertion
* Sudden changes in blood pressure
* Certain medications
The symptoms of TGA are sudden and dramatic, and they can vary in severity. They include:
* Complete loss of memory for events occurring after the onset of the amnesia
* Inability to recall familiar words, names, or faces
* Difficulty learning new information or forming new memories
* Confusion, disorientation, and difficulty recognizing familiar places or objects
TGA is usually diagnosed based on a combination of the following:
* Medical history and physical examination
* Neurological examination to rule out other conditions that may cause similar symptoms
* Imaging tests such as CT or MRI scans to rule out structural brain abnormalities
* Memory testing to assess the extent of memory loss and identify any specific memory deficits
There is no specific treatment for TGA, but supportive care and rehabilitation can help improve the patient's quality of life. Treatment may include:
* Relaxation techniques to reduce stress and anxiety
* Cognitive training to improve memory and cognitive function
* Assistance with daily activities and communication
* Medications to manage related symptoms such as anxiety or sleep disturbances
The prognosis for TGA is generally good, with most patients recovering their memories within a few weeks or months. However, some patients may experience persistent memory loss or other long-term effects. Factors that can influence the prognosis include:
* Age and overall health status
* Severity of the episode
* Presence of any underlying medical conditions
* Response to treatment
There are several lifestyle changes that can help reduce the risk of developing TGA or improve the prognosis:
* Maintain a healthy diet and exercise regularly
* Manage stress and anxiety through relaxation techniques or therapy
* Get enough sleep and practice good sleep hygiene
* Stay mentally active and engage in cognitively stimulating activities
* Avoid alcohol and drugs, especially those that can cause sedation or confusion
In conclusion, TGA is a relatively rare condition that can cause significant memory loss and disorientation. While the prognosis is generally good, early diagnosis and appropriate treatment are essential to improve outcomes. Lifestyle changes such as maintaining a healthy diet, regular exercise, stress management, and cognitive stimulation can also help reduce the risk of developing TGA or improve the prognosis. If you suspect that you or someone else may be experiencing TGA, it is essential to seek medical attention promptly.
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.
The disorder is caused by the damage of brain cells due to the deficiency of thiamine (Vitamin B1) which is essential for proper brain functioning. The condition can be divided into two main categories:
1. Wernicke's Encephalopathy: This is the acute form of the disorder where the individual experiences confusion, ataxia (loss of coordination), and oculomotor dysfunction (abnormal eye movements).
2. Korsakoff's Psychosis: This is the chronic form of the disorder where the individual experiences memory loss and confabulation (making up memories).
Symptoms of Alcohol Amnestic Disorder include:
* Memory loss for events that occurred both short-term and long-term
* Difficulty learning new information
* Confusion and disorientation
* Slurred speech and difficulty with coordination
* Increased risk of seizures
Diagnosis of the disorder is based on a combination of medical history, physical examination, and laboratory tests such as blood tests to check for thiamine deficiency. Treatment typically involves abstinence from alcohol, thiamine supplements, and supportive care to manage symptoms.
Prognosis for Alcohol Amnestic Disorder varies depending on the severity of the condition and the individual's response to treatment. In general, the earlier the diagnosis and treatment, the better the prognosis. However, if left untreated, the condition can lead to permanent brain damage and even death.
It is important to note that Alcohol Amnestic Disorder is preventable by avoiding excessive alcohol consumption and ensuring adequate thiamine intake through a balanced diet or supplements. Early detection and treatment can help to reduce the risk of long-term cognitive impairment and improve overall outcomes.
Example sentence: "The patient experienced a transient ischemic attack, which was caused by a temporary blockage in one of the blood vessels in their brain."
Synonyms: TIA, mini-stroke.
Some common causes of confusion in the medical field include:
1. Medication side effects: Certain medications can cause confusion as a side effect, particularly those that affect the central nervous system, such as sedatives, anti-anxiety drugs, and painkillers.
2. Delirium: A sudden and severe confusional state that can be caused by various factors, such as infections, surgery, or alcohol or drug withdrawal.
3. Dementia: A progressive decline in cognitive function that can cause confusion, memory loss, and difficulty with communication and daily activities. Alzheimer's disease is the most common cause of dementia.
4. Traumatic brain injury: A head injury that can cause confusion, memory loss, and other cognitive difficulties.
5. Stroke: A loss of blood flow to the brain that can cause confusion, weakness, and difficulty with speech and mobility.
6. Infections: Certain infections, such as urinary tract infections or sepsis, can cause confusion and disorientation.
7. Sleep disorders: Sleep disturbances, such as insomnia or sleep apnea, can lead to confusion and other cognitive difficulties.
8. Chronic conditions: Certain chronic conditions, such as diabetes, hypertension, or hypothyroidism, can cause confusion if left untreated or poorly managed.
9. Nutritional deficiencies: Deficiencies in certain nutrients, such as vitamin B12 or thiamine, can cause confusion and other cognitive difficulties.
10. Substance abuse: Withdrawal from drugs or alcohol can cause confusion, agitation, and other cognitive difficulties.
In the medical field, confusion is often evaluated through a series of questions and physical examinations to determine its underlying cause. Treatment may involve addressing any underlying conditions, managing symptoms, and providing supportive care to help improve cognitive function. In some cases, medication or other interventions may be necessary to manage symptoms and improve quality of life.
There are several different types of unconsciousness, including:
1. Concussion: A mild form of traumatic brain injury that can cause temporary unconsciousness, confusion, and amnesia.
2. Coma: A more severe form of unconsciousness that can be caused by a head injury, stroke, or other medical condition. Comas can last for days, weeks, or even months.
3. Vegetative state: A condition in which a person is unaware and unresponsive, but still has some reflexes. This can be caused by a traumatic brain injury, stroke, or other medical condition.
4. Persistent vegetative state (PVS): A long-term version of the vegetative state that can last for months or years.
5. Brain death: A permanent form of unconsciousness that is caused by severe damage to the brain.
Unconsciousness can be diagnosed through a variety of medical tests, including:
1. Neurological exam: A doctor will check the patient's reflexes, muscle strength, and sensation to determine the extent of any brain damage.
2. Imaging tests: CT or MRI scans can help doctors identify any structural abnormalities in the brain that may be causing unconsciousness.
3. Electroencephalogram (EEG): A test that measures electrical activity in the brain to determine if there is any abnormal brain wave activity.
4. Blood tests: To rule out other medical conditions that may be causing unconsciousness, such as infections or poisoning.
Treatment for unconsciousness depends on the underlying cause and can range from simple observation to complex surgical procedures. Some common treatments include:
1. Medications: To control seizures, reduce inflammation, or regulate brain activity.
2. Surgery: To relieve pressure on the brain, repair damaged blood vessels, or remove tumors.
3. Rehabilitation: To help the patient regain lost cognitive and motor function.
4. Supportive care: To address any other medical conditions that may be contributing to the unconsciousness, such as infections or respiratory failure.
Thalamic diseases can result from various causes, including genetic mutations, infections, trauma, and stroke. Some common thalamic diseases include:
1. Thalamic stroke or infarction: This occurs when there is a lack of blood supply to the thalamus, leading to cell death and loss of thalamic function.
2. Thalamic tumors: These are abnormal growths that can develop in the thalamus, either benign or malignant.
3. Thalamic lesions: These are areas of damage or degeneration in the thalamus, which can result from trauma, stroke, or other conditions such as multiple sclerosis.
4. Thalamic migraine: This is a type of migraine that is associated with activation of the thalamus and can cause severe headaches, visual disturbances, and other symptoms.
5. Thalamic pain disorders: These are conditions characterized by chronic pain that is thought to be related to dysfunction in the thalamus.
6. Thalamic sleep disorders: These are conditions that affect the regulation of sleep and wakefulness, such as narcolepsy or insomnia.
7. Thalamic cognitive disorders: These are conditions that affect cognitive function, such as memory loss, attention deficits, and language difficulties.
Thalamic diseases can be challenging to diagnose and treat, as the thalamus is a complex structure that is involved in many brain functions. However, advances in neuroimaging and other diagnostic tools have improved our ability to identify and understand these conditions. Treatment options for thalamic diseases vary depending on the specific condition and can range from medications and lifestyle changes to surgery and other interventions.
Some common types of memory disorders include:
1. Amnesia: A condition where an individual experiences memory loss, either partial or total, due to brain damage or other causes.
2. Dementia: A broad term that describes a decline in cognitive function, including memory loss, confusion, and difficulty with communication and daily activities. Alzheimer's disease is the most common cause of dementia.
3. Mild Cognitive Impairment (MCI): A condition characterized by memory loss and other cognitive symptoms that are more severe than normal age-related changes but not as severe as dementia.
4. Attention Deficit Hyperactivity Disorder (ADHD): A neurodevelopmental disorder that affects attention, impulse control, and hyperactivity. Memory problems are often a component of ADHD.
5. Traumatic Brain Injury (TBI): A condition that occurs when the brain is injured due to a blow or jolt to the head, which can result in memory loss and other cognitive problems.
6. Stroke: A condition where blood flow to the brain is interrupted, leading to brain cell death and potential memory loss.
7. Meningitis: An inflammatory condition that affects the membranes covering the brain and spinal cord, which can lead to memory loss and other cognitive problems.
8. Encephalitis: An inflammatory condition that affects the brain directly, leading to memory loss and other cognitive problems.
9. Chronic Fatigue Syndrome (CFS): A condition characterized by persistent fatigue, memory loss, and other cognitive symptoms.
10. Sleep Disorders: Sleep disturbances can affect memory and cognitive function, including conditions such as insomnia, sleep apnea, and restless leg syndrome.
The diagnosis of memory disorders typically involves a combination of medical history, physical examination, laboratory tests, and neuropsychological evaluations. The specific treatment approach will depend on the underlying cause of the memory loss, but may include medication, behavioral interventions, and lifestyle changes.
In medical terms, craniocerebral trauma is defined as any injury that affects the skull, brain, or both, as a result of an external force. This can include fractures of the skull, intracranial hemorrhages (bleeding inside the skull), and diffuse axonal injuries (DAI), which are tears in the fibers of the brain.
Craniocerebral trauma can be classified into two main categories: closed head injury and open head injury. Closed head injury occurs when the skull does not fracture, but the brain is still affected by the impact, such as from whiplash or shaking. Open head injury, on the other hand, involves a fracture of the skull, which can cause the brain to be exposed to the outside environment and increase the risk of infection.
Treatment for craniocerebral trauma depends on the severity of the injury and may include observation, medication, surgery, or a combination of these. In severe cases, craniocerebral trauma can lead to long-term cognitive, emotional, and physical impairments, and may require ongoing rehabilitation and support.
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.
Some common causes of chronic brain damage include:
1. Traumatic brain injury (TBI): A blow to the head or other traumatic injury that causes the brain to bounce or twist inside the skull, leading to damage to brain cells and tissues.
2. Stroke or cerebral vasculature disorders: A loss of blood flow to the brain due to a blockage or rupture of blood vessels, leading to cell death and tissue damage.
3. Infections such as meningitis or encephalitis: Inflammation of the brain and its membranes caused by viral or bacterial infections, which can lead to damage to brain cells and tissues.
4. Chronic exposure to toxins, such as pesticides or heavy metals: Prolonged exposure to these substances can damage brain cells and tissues over time.
5. Neurodegenerative diseases, such as Alzheimer's disease or Parkinson's disease: These conditions are characterized by the progressive loss of brain cells and tissue, leading to cognitive decline and other symptoms.
The effects of chronic brain damage can vary depending on the location and severity of the damage. Some common effects include:
1. Cognitive impairments: Difficulty with memory, attention, problem-solving, and other cognitive functions.
2. Emotional and behavioral changes: Depression, anxiety, irritability, and mood swings.
3. Physical symptoms: Weakness or paralysis on one side of the body, difficulty with balance and coordination, and changes in sensation or perception.
4. Communication difficulties: Slurred speech, difficulty finding the right words, and trouble understanding spoken language.
5. Social and occupational impairments: Difficulty with daily activities, social interactions, and work-related tasks.
The good news is that there are several strategies that can help mitigate the effects of chronic brain damage. These include:
1. Physical exercise: Regular physical activity has been shown to promote brain health and reduce the risk of cognitive decline.
2. Cognitive stimulation: Engaging in mentally challenging activities, such as reading, puzzles, or learning a new skill, can help build cognitive reserve and reduce the risk of cognitive decline.
3. Social engagement: Building and maintaining social connections has been shown to promote brain health and reduce the risk of cognitive decline.
4. Stress management: Chronic stress can exacerbate brain damage, so finding ways to manage stress, such as through meditation or exercise, is important.
5. Proper nutrition: Eating a diet rich in fruits, vegetables, and omega-3 fatty acids can help support brain health and reduce the risk of cognitive decline.
6. Medication and therapy: In some cases, medication or therapy may be necessary to manage the symptoms of chronic brain damage.
7. Neuroplasticity-based interventions: Techniques that promote neuroplasticity, such as non-invasive brain stimulation, can help improve cognitive function and reduce the risk of cognitive decline.
It's important to note that these strategies may not reverse chronic brain damage, but they can help mitigate its effects and improve overall brain health. If you suspect that you or someone you know may be experiencing chronic brain damage, it is important to seek medical attention as soon as possible. Early diagnosis and treatment can help reduce the risk of long-term cognitive decline and improve quality of life.
The symptoms of MPD/DID can vary widely and may include:
1. Memory loss or gaps: Individuals with MPD/DID may experience significant memory lapses or gaps, especially for events that occurred while they were in a different personality state.
2. Identity confusion: They may feel uncertain about their own identity or may experience shifts in their sense of self.
3. Time distortion: They may experience time distortions, such as feeling like time is speeding up or slowing down.
4. Depersonalization: They may feel detached from themselves or from their body.
5. Derealization: They may feel detached from the world around them.
6. Amnesia: They may experience amnesia for important information, especially if it is related to traumatic events.
7. Identity fragmentation: They may experience a sense of fragmentation or disintegration of their identity.
8. Self-destructive behaviors: They may engage in self-destructive behaviors, such as self-harm or substance abuse.
9. Emotional dysregulation: They may experience intense and unpredictable mood swings.
10. Dissociation: They may experience dissociation, which is a feeling of being disconnected from oneself or the world around them.
The exact cause of MPD/DID is not fully understood, but it is thought to be related to traumatic events, such as childhood abuse or neglect, that can lead to dissociation as a coping mechanism. Treatment typically involves therapy and may include medication to help manage symptoms such as anxiety or depression.
Synonyms: Castration-resistant prostatic neoplasm, Hormone-refractory prostate cancer, Androgen-independent prostate cancer
Example sentence: "The patient's prostate cancer had progressed to castration-resistant prostatic neoplasms, and he was experiencing severe bone pain despite undergoing multiple treatments."
Malignant prostatic neoplasms are cancerous tumors that can be aggressive and spread to other parts of the body (metastasize). The most common type of malignant prostatic neoplasm is adenocarcinoma of the prostate, which accounts for approximately 95% of all prostate cancers. Other types of malignant prostatic neoplasms include sarcomas and small cell carcinomas.
Prostatic neoplasms can be diagnosed through a variety of tests such as digital rectal examination (DRE), prostate-specific antigen (PSA) test, imaging studies (ultrasound, CT scan or MRI), and biopsy. Treatment options for prostatic neoplasms depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health. Treatment options can include active surveillance, surgery (robotic-assisted laparoscopic prostatectomy or open prostatectomy), radiation therapy (external beam radiation therapy or brachytherapy), and hormone therapy.
In summary, Prostatic Neoplasms are tumors that occur in the prostate gland, which can be benign or malignant. The most common types of malignant prostatic neoplasms are adenocarcinoma of the prostate, and other types include sarcomas and small cell carcinomas. Diagnosis is done through a variety of tests, and treatment options depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health.
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- Amnesia retrograde. (lookformedical.com)
- Pathologic partial or complete loss of the ability to recall past experiences (AMNESIA, RETROGRADE) or to form new memories (AMNESIA, ANTEROGRADE). (lookformedical.com)
- We describe the case of a 60-year-old woman who presented with acute onset, recent retrograde, and anterograde amnesia characteristic of TGA. (stanfordhealthcare.org)
- Anterograde, Retrograde, and Post-Traumatic Amnesia. (inrseminars.com)
- Retrograde amnesia, the loss of pre-existing memories targets the patient's most recent memories. (ivaluehealth.net)
- Clinical research in the diagnosis, early treatment, and secondary prevention of cerebrovascular diseases including ischemic stroke, transient ischemic attach, intracerebral hemorrhage, and subarachnoid hemorrhage, with a special focus on quality improvement, disparity of care and minorities. (healthpartners.com)
- 3 Other reported conditions that have not systematically been asked about include other acute ischemic heart disease (baseline: n=6, unknown timing: n=33, incident: n=248), chronic ischemic heart disease (baseline: n=12, unknown timing: n=139, incident: n=617), and transient global amnesia (baseline: n=1, unknown timing: n=2, incident: n=34). (nih.gov)
Types of Amnesia1
- There are many types of amnesia. (ivaluehealth.net)
- Anterograde amnesia is the loss of long-term memory, the loss of the ability to form new memories through memorization. (ivaluehealth.net)
- Dissociative Amnesia (DSM-5) and Multiple Personality (Dissociative Identity Disorder). (inrseminars.com)
- Post-traumatic amnesia usually occurs after a head injury, dissociative amnesia is due to a psychological cause and includes: repressed memory, dissociative fugue, post-hypnotic amnesia. (ivaluehealth.net)
- Delirium, dementia, amnesia (and certain other alterations in cognition, judgment, and/or memory) are grouped together in this article as organically based disruptions of brain functioning. (medscape.com)
- 1. Transient global amnesia: diffusion-weighted imaging lesions and cerebrovascular disease. (nih.gov)
- 9. Transient global amnesia and focal diffusion weighted imaging lesions in mesiotemporal region: A ten-year experience. (nih.gov)
- 14. Long-term sequelae of hippocampal lesions in patients with transient global amnesia: A multiparametric MRI study. (nih.gov)
- 17. Bilateral Hippocampal DWI Lesions in Transient Global Amnesia. (nih.gov)
- Unilateral lesions of the fornix rarely cause amnesia and have not previously been reported to be associated with the distinctive amnesic picture of TGA. (stanfordhealthcare.org)
- According to the paper, he has been diagnosed with Transient Global Amnesia, an inability to make new memories, and as well as being in a fugue state , a kind of blackout that can cause people to wander away from home unexpectedly and create new identities. (popsci.com)
- Transient Global Amnesia -which Boatwright has also been diagnosed with-is characterized by a temporary, abrupt inability to make new memories , without any other neurological disfunction clouding consciousness, perception or identity. (popsci.com)
- A syndrome characterized by a transient loss of the ability to form new memories. (nih.gov)
- [ 1 ] Delirium is usually transient, but it can be persistent leading to a chronically dementing process in elderly patients. (medscape.com)
- 6. Bilateral hippocampal abnormalities on diffusion-weighted MRI in transient global amnesia: report of a case. (nih.gov)
- Memory loss, also called amnesia, is a state characterized by an abnormal degree of forgetfulness and/or inability to remember past events. (ivaluehealth.net)
- Lacunar amnesia is the loss of memory about one particular event and childhood amnesia is the inability to remember events from one's own childhood. (ivaluehealth.net)
- Stroke is an extremely uncommon cause of transient global amnesia (TGA). (stanfordhealthcare.org)
- I's a temporary bout of amnesia, usually lasting for a few days or perhaps weeks, that often induces someone to drop whatever they're doing and wander away from home or work. (popsci.com)
- Real amnestics rarely if ever forget their own names.Organic amnesia is caused by brain damage-sometimes from seizures, brain inflammation or diseases like Alzheimer's. (popsci.com)
- Organic amnesia, resulting from brain damage , don't usually make people forget who they are. (popsci.com)
- Organic forms of amnesia are usually associated with dysfunction of the DIENCEPHALON or HIPPOCAMPUS. (lookformedical.com)
- 7. Selective affection of hippocampal CA-1 neurons in patients with transient global amnesia without long-term sequelae. (nih.gov)
- 12. Vascular Risk Factors and Internal Jugular Venous Flow in Transient Global Amnesia: A Study of 165 Japanese Patients. (nih.gov)
- 15. Long-term outcome in transient global amnesia patients with and without focal hyperintensities in the CA1 region of the hippocampus. (nih.gov)
- 16. Relationship between Cytotoxicity in the Hippocampus and an Abnormal High Intensity Area on the Diffusion-weighted Images of Three Patients with Transient Global Amnesia. (nih.gov)
- He underwent surgery to treat severe epileptic seizures in the 1950s, and due to the removal of part of the medial temporal region of his brain, exhibited profound amnesia for the rest of his life. (popsci.com)
- Severe declarative amnesia and concomitant deficits in executive function result in compromised autonomy. (seekhealthz.com)
- 4. Clinical experience of modified diffusion-weighted imaging protocol for lesion detection in transient global amnesia: an 8-year large-scale clinical study. (nih.gov)
- 5. Frequency of silent brain infarction in transient global amnesia. (nih.gov)
- There are two broader categories of amnesias: those caused by physical trauma in the brain, and those caused by a psychological issue. (popsci.com)
- Memory appears to be stored in several parts of the limbic system of the brain, and any condition that interferes with the function of this system can cause amnesia. (ivaluehealth.net)
- Source amnesia is a memory disorder in which someone can recall certain information, but they do not know where or how they obtained the information. (ivaluehealth.net)
- Transient global amnesia associated with a unilateral infarction of the fornix: case report and review of the literature. (stanfordhealthcare.org)
- Drug-induced amnesia is intentionally caused by injection of an amnesiac drug to help a patient forget surgery or medical procedures. (ivaluehealth.net)
- The memory loss may be for a short time and then resolve (transient). (medlineplus.gov)
- During the period of amnesia, immediate and recent memory abilities are impaired, but the level of consciousness and ability to perform other intellectual tasks are preserved. (nih.gov)