Related Experiment Video
Updated: Aug 8, 2026
10:31
Three-dimensional Imaging and Analysis of Mitochondria within Human Intraepidermal Nerve Fibers
Published on: September 29, 2017
Thiamine deficiency neuropathy. It's still common today
1James A. Haley Veterans Hospital, Tampa, FL 33612.
Postgraduate Medicine
|June 1, 1989
Summary
Thiamine deficiency neuropathy is rising but often missed. Early diagnosis through a high index of suspicion and electrophysiologic studies is crucial for effective treatment.
Area of Science:
- Neurology
- Nutritional Neuroscience
Background:
- Thiamine deficiency neuropathy is increasingly prevalent.
- This neurological disorder is frequently underdiagnosed in clinical practice.
Observation:
- Common symptoms like weakness and burning feet are often dismissed as minor complaints.
- Electrophysiologic studies offer sensitive and supportive diagnostic evidence.
Findings:
- A high index of suspicion is essential for timely diagnosis.
- Early detection facilitates more successful therapeutic interventions.
Implications:
- Improved diagnostic strategies are needed for thiamine deficiency neuropathy.
- Recognizing subtle symptoms and utilizing electrophysiology can improve patient outcomes.
Related Concept Videos
01:30Vitamins
Vitamins, derived from the Latin word for life, are essential organic substances required in small quantities for optimal growth and overall well-being. Unlike other organic nutrients, vitamins don't act as sources of energy or building materials but rather facilitate these nutrients' utilization by the body. Vitamins are predominantly coenzymes, assisting enzymes in specific chemical actions, like the oxidation of glucose for energy involving B vitamins. Most vitamins are not produced in our...
01:26Type I Diabetes II: Pathophysiology
Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
01:19Type I Diabetes III: Clinical Manifestations
Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the kidneys...
01:24Type II Diabetes II: Pathophysiology
PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
01:22Diabetic Neuropathy
DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
01:23Alzheimer Disease ll: Pathophysiology
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...