Dementia with Lewy bodies

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Dementia with Lewy bodies

BMB2

BMB2

Seizures: Pathology review
Seizures: Clinical
Febrile seizure
Seizures and epilepsy
Early infantile epileptic encephalopathy (NORD)
Nonbenzodiazepine anticonvulsants
Migraine medications
Migraine
Neuron action potential
Resting membrane potential
Concussion and traumatic brain injury
Sleep
Sleep disorders: Clinical
Anticonvulsants and anxiolytics: Barbiturates
Anticonvulsants and anxiolytics: Benzodiazepines
Essential tremor
Malingering, factitious disorders and somatoform disorders: Pathology review
Somatic symptom disorders: Clinical
Somatic symptom disorder
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Dissociative disorders: Clinical
Amnesia, dissociative disorders and delirium: Pathology review
Narcolepsy (NORD)
Psychomotor stimulants
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Muscle weakness: Clinical
Myalgias and myositis: Pathology review
Fibromyalgia
Diabetic nephropathy
Tricyclic antidepressants
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Medications for neurodegenerative diseases
Toxidromes: Clinical
Body focused repetitive disorders
Headaches: Clinical
Demyelinating disorders: Pathology review
Serotonin and norepinephrine reuptake inhibitors
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Lead poisoning
Hemolytic-uremic syndrome
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Monoclonal gammopathy of undetermined significance
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Inflammatory myopathies: Clinical
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Myotonic dystrophy
Memory palaces
Herpes simplex virus
Neuromuscular junction and motor unit
Slow twitch and fast twitch muscle fibers
Muscle contraction
Development of the muscular system
Development of the axial skeleton
Patellar tendon rupture
Achilles tendon rupture
Lower back pain: Clinical
Carpal tunnel syndrome
Radial head subluxation (Nursemaid elbow)
Bell palsy
Headaches: Pathology review
Cluster headache
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Epidural hematoma
Traumatic brain injury: Clinical
Intracerebral hemorrhage
Subarachnoid hemorrhage
Subdural hematoma
Traumatic brain injury: Pathology review
Idiopathic intracranial hypertension
Vasculitis
Vasculitis: Clinical
Dementia with Lewy bodies
Spinocerebellar ataxia (NORD)
Amyloidosis
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Dementia and delirium: Clinical
Frontotemporal dementia
Dementia: Pathology review
Hypokinetic movement disorders: Clinical
Alzheimer disease
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Delirium
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Hyperkinetic movement disorders: Clinical
Back pain: Pathology review
Stroke: Clinical
Compartment syndrome
Macrocytic anemia: Pathology review
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Hyperkalemia: Clinical
Hypothesis testing: One-tailed and two-tailed tests
Paired t-test
One-way ANOVA
Two-way ANOVA
Type I and type II errors
Two-sample t-test
Correlation
Repeated measures ANOVA
Meningitis, encephalitis and brain abscesses: Clinical
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Clostridium tetani (Tetanus)
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Encephalitis
Eastern and Western equine encephalitis virus
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Knowledge Shot: What is acute flaccid myelitis, the polio-like paralyzing disease
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Angiostrongylus (Eosinophilic meningitis)
Varicella zoster virus
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Measles virus
Central nervous system infections: Pathology review
Meningitis, encephalitis and brain abscesses: Clinical
Adult brain tumors
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Adult brain tumors: Pathology review
Pediatric brain tumors
Brain tumors: Clinical
Multiple sclerosis
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Ataxia-telangiectasia
Huntington disease
Opsoclonus myoclonus syndrome (NORD)
Primary ciliary dyskinesia
Brain herniation
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Multiple myeloma

Transcript

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Lewy body dementia is a type of dementia, where individuals lose their memory and have difficulty learning new information.

Lewy bodies refers to protein deposits found inside neurons, and they’re named after Frederic Lewy, the neurologist who discovered them.

Lewy body dementia is a neurodegenerative disease, meaning that it worsens over time, and it’s the disease that afflicted comedian and actor Robin Williams.

The brain is made up of billions of neurons that communicate with each other by releasing neurotransmitters.

Most neurons in the cerebral cortex are called cholinergic neurons because they produce acetylcholine.

In contrast, neurons in a section of the midbrain called the substantia nigra are in charge of initiating movement and other motor functions.

These neurons are called dopaminergic because they produce dopamine.

The underlying cause of Lewy body dementia isn’t well understood.

Normally, neurons contain a protein called alpha synuclein, and in Lewy body dementia, this protein gets misfolded within the neurons.

The misfolded alpha-synuclein aggregates to form Lewy bodies that deposit inside neurons, particularly in the cortex and the substantia nigra.

Under a microscope, Lewy bodies look like dark, eosinophilic inclusions inside the affected neurons.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "Neuroimaging in Lewy body dementia" Journal of Neurology (2018)
  5. "Lewy body dementias" The Lancet (2015)
  6. "Dysfunctional brain dynamics and their origin in Lewy body dementia" Brain (2019)