Wernicke Encephalopathy
Thiamine Deficiency
Thyroid Crisis
Thyrotoxicosis
Hepatic Encephalopathy
Magnetic Resonance Imaging
Brain
Aphasia, Wernicke
Encephalopathy, Bovine Spongiform
Degeneration of anterior thalamic nuclei differentiates alcoholics with amnesia. (1/101)
The specific neural substrate underlying the amnesia in alcoholic Korsakoff's psychosis is poorly defined because of the considerable brain damage found in many non-amnesic alcoholics, particularly those with Wernicke's encephalopathy. Using operational criteria to identify alcoholics with and without Korsakoff's psychosis, we have shown that many of the cortical and subcortical regions involved in the encoding and retrieval of episodic memory are either unaffected (hippocampus) or damaged to the same extent (prefrontal cortex and the cholinergic basal forebrain) in both amnesic and non-amnesic alcoholics. In the present study we analysed the diencephalic regions involved in episodic memory to determine the neural substrate for the amnesia observed in alcoholic Korsakoff's psychosis. The number of neurons in spaced serial sections containing the hypothalamic mamillary nuclei and the anterior and mediodorsal thalamic nuclei was estimated using unbiased stereological techniques. Neurodegeneration of the hypothalamic mamillary nuclei and the mediodorsal thalamic nuclei was substantial in both non-amnesic and amnesic alcoholics with Wernicke's encephalopathy. However, neuronal loss in the anterior thalamic nuclei was found consistently only in alcoholic Korsakoff's psychosis. This is the first demonstration of a differentiating lesion in alcoholic Korsakoff's psychosis and supports previous evidence that degeneration of thalamic relays are important in this memory disorder. (+info)A survey of the current clinical practice of psychiatrists and accident and emergency specialists in the United Kingdom concerning vitamin supplementation for chronic alcohol misusers. (2/101)
Although it is well known that B-vitamin deficiencies directly affecting the brain are common in alcohol misuse, no concise guidelines on the use of vitamin supplements in alcohol misusers currently exist in the UK. The purpose of this study was to assess current practice and opinion among UK physicians. Questionnaires were completed by a total of 427 physicians comprising Accident and Emergency (A&E) specialists and psychiatrists, with a response rate of 25%. The main findings were that vitamin deficiency was perceived as being uncommon amongst alcohol misusers (<25%) and there was no consensus as to which B vitamins are beneficial in treatment or the best method of administration of B-vitamin supplementation. The majority of psychiatrists favoured oral administration for prophylaxis against the Wernicke-Korsakoff syndrome in chronic alcohol misusers and parenteral therapy in patients with signs of Wernicke-Korsakoff syndrome. Whilst only just over half the A&E specialists expressed a preference, most favoured parenteral therapy in both cases. Most respondents did not currently have a unit policy/protocol on the management of vitamin supplementation in chronic alcohol misusers. Overall, the findings suggest that there is wide variation in current practice and highlight the need for guidelines in this area. (+info)Neuropathological findings after bone marrow transplantation: an autopsy study of 180 cases. (3/101)
We prospectively evaluated the neuropathological complications of 180 patients who underwent autopsy studies following bone marrow transplantation (BMT) (177 allogeneic, three autologous). The most frequent underlying disorders included severe aplastic anemia (n = 55), chronic myelogenous leukemia (n = 53), acute myelogenous leukemia (n = 24) and Fanconi anemia (n = 16). There were 114 males and 66 females. Neuropathological findings were detected in 90.55% of the patients. The most frequent findings were subarachnoid hemorrhages (SAH) (n = 57), intraparenchymal hemorrhages (IHP) (n = 49), fungal infections (n = 16), Wernicke's encephalopathy (n = 10), microglial nodular encephalopathy (n = 10) and neurotoxoplasmosis (n = 8). In only 17 patients was the brain within normal limits. Survival time after BMT averaged 5.4 months and the majority of patients died in the first 3 months post BMT (n = 105). Central nervous system (CNS) pathology was the main cause of death in 17% of the patients (n = 31), with a predominance of IHP in this particular group. Furthermore, the survival time of these patients who died of CNS causes (96.3 days) was almost half of the survival time of those who died of extra-cerebral causes (177.8 days) (P = 0.0162). IHP (70. 96 vs27.22%) (P < 0.001), fungal infections (25.8 vs 8.88%) (P < 0. 001) and toxoplasmosis (9.67 vs 4.44%) (P < 0.001) were significantly more frequent in the group of patients who died due to CNS causes than in the control group. The findings of this work provide a possible guide to the possible causes of neurological syndromes following BMT. Bone Marrow Transplantation (2000) 25, 301-307. (+info)Gestational thyrotoxicosis with acute Wernicke encephalopathy: a case report. (4/101)
A 35-year-old hyperthyroid woman who developed nausea, vomiting, tachycardia, nystagmus and mental disturbance, was referred to our hospital with a suspected diagnosis of thyroid storm. However, the thyroid gland was only slightly palpable, bruits were not audible, and exophthalmos was not present. Serum levels of thyroid hormone were increased, but TSH receptor antibodies were negative. Echography and color flow doppler ultrasonography revealed a slightly enlarged thyroid gland and a slightly increased blood flow, both of which were much less milder than those expected for severe hyperthyroid Graves' disease. Under the diagnosis of hyperthyroidism due to gestational thyrotoxicosis associated with Wernicke encephalopathy, vitamin B1 was administered on the first day of admission. Her consciousness became nearly normal on the second day except for slight amnesia. Her right abducent nerve palsy rapidly improved, but horizontal and vertical nystagmus, diminished deep tendon reflexes and gait ataxia improved only gradually. MRI findings of the brain were compatible with acute Wernicke encephalopathy. We concluded that history taking and physical findings are important to make a differential diagnosis of gestational thyrotoxicosis with acute Wernicke encephalopathy from Graves' thyroid storm, and that Wernicke encephalopathy should be treated as soon as possible to improve the prognosis. (+info)High ethanol intake and malnutrition in alcoholic cerebellar shrinkage. (5/101)
To determine the influence of chronic ethanol intake and nutritional status on cerebellar shrinkage in alcoholism, we studied 12 undernourished patients with acute Wernicke's encephalopathy (WE), 12 undernourished and 24 well-nourished asymptomatic chronic alcoholics, and 24 age-matched well-nourished controls, using morphometric analysis of MRI scans with volumetry of the cerebellum. Alcoholics reported a mean daily intake of ethanol of 177+/-8 g over a period of 27+/-1 years. Most undernourished alcoholics and half of the well-nourished alcoholics, compared to one-tenth of the controls, showed a significant reduction in cerebellar volume (p< or =0.01, both). Alcoholics with cerebellar shrinkage (n=33) were older (p=0.05) and tended to report greater daily ethanol intake than alcoholics without cerebellar shrinkage (n=15), although not significantly so (p=0.09). Cerebellar volume correlated negatively with age in controls and asymptomatic alcoholics (r> or =0.52, p< or =0.01, both), with a significantly greater shrinkage for age in the latter (p=0.003). Logistic regression analysis showed that malnutrition (OR 6.6 [95%CI 1.7-25.6], p=0.005) and a daily ethanol intake of more than 140 g over ten years (OR 6.1 [95%CI 1.8-20.5], p=0.003) were independently associated with the development of cerebellar shrinkage. (+info)Wernicke's encephalopathy: atypical manifestation at MR imaging. (6/101)
SUMMARY: We report a case of atypical manifestation of hyperintense lesions in a 64-year-old female patient with Wernicke's encephalopathy. Fluid-attenuated inversion recovery and T2-weighted images demonstrated symmetrical distribution of hyperintense lesions in cerebellar dentate nuclei, tegmentum of the lower pons, red nuclei, and tectum of the midbrain, and T1-weighted sagittal images showed atrophy of the mamillary bodies. The hyperintense lesions were completely resolved on follow-up MR images. (+info)Diffusion-weighted imaging in a case of wernicke encephalopathy. (7/101)
In a chronic alcoholic patient with progressive confusion, which was consistent with the clinical diagnosis of Wernicke encephalopathy, T2-weighted, FLAIR and diffusion weighted (DWI) MR imaging depicted brain abnormalities located in both medial thalamic nuclei. Apparent Diffusion Coefficient (ADC) measurements in these regions shown unexpected normal values, referring to Wernicke pathological findings and DWI data. DWI may be helpful to diagnose early basal nuclei abnormalities, but may fail to compute ADC values in these locations. (+info)Wernicke's encephalopathy presenting with severe dysphagia: a case report. (8/101)
A 62-year-old man developed dysphagia 4 weeks before the classic symptoms and signs of Wernicke's encephalopathy appeared. Adequate treatment with parenteral thiamine resulted in complete recovery of all symptoms, including his dysphagia. This extraordinary presentation with dysphagia, and the unusual course of the disease, encouraged us to present this case history. (+info)Wernicke Encephalopathy is a neuropsychiatric disorder that is caused by a deficiency of thiamine (vitamin B1). It is characterized by a classic triad of symptoms: confusion, oculomotor dysfunction (such as nystagmus and ophthalmoplegia), and gait ataxia. Other symptoms can include memory loss, apathy, and hypothermia.
Wernicke Encephalopathy is most commonly seen in alcoholics due to poor nutrition, but it can also occur in people with conditions that cause malabsorption or increased thiamine requirements, such as AIDS, cancer, and chronic diarrhea. Immediate treatment with thiamine replacement therapy is necessary to prevent progression of the disease and potential permanent neurological damage. If left untreated, Wernicke Encephalopathy can lead to Korsakoff's syndrome, a chronic memory disorder.
Thiamine deficiency, also known as beriberi, is a condition that results from inadequate intake or impaired absorption of thiamine (vitamin B1), which is essential for energy metabolism and nerve function. This deficiency can lead to various symptoms such as peripheral neuropathy, muscle weakness, heart failure, and in severe cases, Wernicke-Korsakoff syndrome, a neurological disorder associated with alcoholism. Thiamine deficiency is commonly found in populations with poor nutrition, alcohol dependence, and gastrointestinal disorders affecting nutrient absorption.
Thiamine, also known as vitamin B1, is a water-soluble vitamin that plays a crucial role in certain metabolic reactions, particularly in the conversion of carbohydrates into energy in the body. It is essential for the proper functioning of the heart, nerves, and digestive system. Thiamine acts as a cofactor for enzymes involved in the synthesis of neurotransmitters and the metabolism of carbohydrates, lipids, and proteins. Deficiency in thiamine can lead to serious health complications, such as beriberi (a disease characterized by peripheral neuropathy, muscle wasting, and heart failure) and Wernicke-Korsakoff syndrome (a neurological disorder often seen in alcoholics due to chronic thiamine deficiency). Thiamine is found in various foods, including whole grains, legumes, pork, beef, and fortified foods.
A thyroid crisis, also known as thyrotoxic crisis or storm, is a rare but life-threatening condition characterized by an exaggerated response to the excess production of thyroid hormones (thyrotoxicosis). This condition can lead to severe hypermetabolic state, multi-organ dysfunction, and cardiovascular collapse if not promptly diagnosed and treated.
Thyroid crisis is often triggered by a stressful event, infection, or surgery in individuals with uncontrolled or poorly managed hyperthyroidism, particularly those with Graves' disease. The symptoms of thyroid crisis include high fever, tachycardia (rapid heart rate), hypertension (high blood pressure), agitation, confusion, delirium, vomiting, diarrhea, and sometimes coma.
The diagnosis of thyroid crisis is based on the clinical presentation, laboratory tests, and imaging studies. Treatment typically involves hospitalization in an intensive care unit, administration of medications to block the production and release of thyroid hormones, control heart rate and rhythm, correct electrolyte imbalances, and provide supportive care until the patient's condition stabilizes.
Thyrotoxicosis is a medical condition that results from an excess of thyroid hormones in the body, leading to an overactive metabolic state. It can be caused by various factors such as Graves' disease, toxic adenoma, Plummer's disease, or excessive intake of thyroid hormone medication. Symptoms may include rapid heart rate, weight loss, heat intolerance, tremors, and increased sweating, among others. Thyrotoxicosis is not a diagnosis itself but a manifestation of various underlying thyroid disorders. Proper diagnosis and management are crucial to prevent complications and improve quality of life.
Hepatic encephalopathy (HE) is a neuropsychiatric syndrome associated with liver dysfunction and/or portosystemic shunting. It results from the accumulation of toxic substances, such as ammonia and inflammatory mediators, which are normally metabolized by the liver. HE can present with a wide range of symptoms, including changes in sleep-wake cycle, altered mental status, confusion, disorientation, asterixis (flapping tremor), and in severe cases, coma. The diagnosis is based on clinical evaluation, neuropsychological testing, and exclusion of other causes of cognitive impairment. Treatment typically involves addressing the underlying liver dysfunction, reducing ammonia production through dietary modifications and medications, and preventing further episodes with lactulose or rifaximin therapy.
Medical Definition:
Magnetic Resonance Imaging (MRI) is a non-invasive diagnostic imaging technique that uses a strong magnetic field and radio waves to create detailed cross-sectional or three-dimensional images of the internal structures of the body. The patient lies within a large, cylindrical magnet, and the scanner detects changes in the direction of the magnetic field caused by protons in the body. These changes are then converted into detailed images that help medical professionals to diagnose and monitor various medical conditions, such as tumors, injuries, or diseases affecting the brain, spinal cord, heart, blood vessels, joints, and other internal organs. MRI does not use radiation like computed tomography (CT) scans.
The brain is the central organ of the nervous system, responsible for receiving and processing sensory information, regulating vital functions, and controlling behavior, movement, and cognition. It is divided into several distinct regions, each with specific functions:
1. Cerebrum: The largest part of the brain, responsible for higher cognitive functions such as thinking, learning, memory, language, and perception. It is divided into two hemispheres, each controlling the opposite side of the body.
2. Cerebellum: Located at the back of the brain, it is responsible for coordinating muscle movements, maintaining balance, and fine-tuning motor skills.
3. Brainstem: Connects the cerebrum and cerebellum to the spinal cord, controlling vital functions such as breathing, heart rate, and blood pressure. It also serves as a relay center for sensory information and motor commands between the brain and the rest of the body.
4. Diencephalon: A region that includes the thalamus (a major sensory relay station) and hypothalamus (regulates hormones, temperature, hunger, thirst, and sleep).
5. Limbic system: A group of structures involved in emotional processing, memory formation, and motivation, including the hippocampus, amygdala, and cingulate gyrus.
The brain is composed of billions of interconnected neurons that communicate through electrical and chemical signals. It is protected by the skull and surrounded by three layers of membranes called meninges, as well as cerebrospinal fluid that provides cushioning and nutrients.
Wernicke's aphasia is a type of fluent aphasia, also known as receptive or sensory aphasia. It is named after the neurologist Carl Wernicke. This type of aphasia is caused by damage to the posterior portion of the left superior temporal gyrus (Wernicke's area) in the dominant hemisphere of the brain, typically as a result of stroke or head injury.
Individuals with Wernicke's aphasia have difficulty understanding spoken or written language. They may speak in long, grammatically correct sentences that are filled with incorrect or made-up words (neologisms) and have little meaning. They are often unaware of their errors and have poor comprehension of both spoken and written language. This can lead to significant difficulties in communication and can be very frustrating for the person with aphasia and their communication partners.
Treatment for Wernicke's aphasia typically involves speech-language therapy, which may focus on improving comprehension, expression, reading, and writing skills. The prognosis for recovery varies depending on the severity of the brain injury and the individual's overall health and cognitive status.
Bovine spongiform encephalopathy (BSE), also known as "mad cow disease," is a progressive neurodegenerative disorder that affects cattle. It is caused by prions, which are misfolded proteins that can cause other proteins in the brain to also misfold and accumulate, leading to brain damage and degeneration. The disease is named for the sponge-like appearance of the brain tissue that results from this degenerative process.
BSE is a zoonotic disease, which means that it can be transmitted from animals to humans. In humans, BSE is known as variant Creutzfeldt-Jakob disease (vCJD) and is caused by consuming contaminated beef products. The symptoms of vCJD include rapidly progressing dementia, neurological symptoms such as muscle spasms and difficulty coordinating movements, and physical deterioration leading to death.
It's important to note that the use of certain growth promoters in cattle feed and the practice of feeding cattle meat and bone meal have been banned in many countries in order to prevent the spread of BSE. Additionally, strict controls on the inspection and testing of beef products have been implemented to ensure their safety.