4th Exam: Neurologic Disease Flashcards
Meningococcal Meningitis:
Carriers have nasopharyngeal bacteria, often in epidemics, outbreaks, young adults and kids, DIC = intravascular thrombosis (caps) (skin, adrenal lesions), can be fatal
Meningitis with WFS:
Adrenal gland hemorrhage = insufficiency, meningitis assoc w inflammation, inflammation → leaky vessels→ edema, seizures, confusion, coma, WFS: numerous skin hemorrhages
WFS sf:
Waterhouse-Friderichsen Syndrome
Brain Abscess sources:
local or distant infection
o Endocarditis, tooth extraction
• Endocarditis: emboli on valves travel to brain
Etiology of brain abscess:
usually bacterial, not a single species, but mixed flora
Signs of brain abscess:
signs of mass lesion w fever, headache, sizures, elevated WBC
Mortality, morbidity of brain abscesses:
10%, 50%
Abscess:
necrosis of tissue + inflammation, PMNs
What forms the capsule around an abscess?
collagen
Why does a capsule form around an abscess?
Attempt to wall-off infection and prevent spread
Myotonic Dystrophy:
Hatchet face with ptosis (droopy eyelids), dysphagia (be aware, may choke on saliva), muscle disease, dominant inheritance, progressive muscle weakness
Mito Disorders esp effect:
cells in organs that don’t turn over quickly (heart, skeletal muscle, brain)
Mito Myopathies:
Ptosis, dysphagia, too many mito, abnormal mitochondria
Abnormal mitochondria:
Differing sizes & shapes, whorled appearance (whirling cristae), crystal-like inclusions
Degenerative Diseases:
Selective vulnerability: distinct topography, often Idiopathic, hereditary/genetic/molecular basis, neurons primarily affected, atrophy + gliosis (astrocytes proliferate → scarring of the brain) + a unique change
Dementia:
Loss of cognitive function, decline from a previous level of function, slowly progressive, modalities affected: memory, judgment, reasoning, calculation, language, lesions in cerebrum
Causes of dementia:
Alzheimer’s & similar diseases, Huntington’s, Parkinson’s (movement disorders), vascular disease, infections, alcohol abuse, Vit deficiency
Alzheimer’s:
- 50-75% of all dementia cases
- Incidence increases w age
o 50% people > 85yo - 5-10yr survival after dx
- Disease of cerebral cortex- cerebral cortical atrophy, diffuse
- Senile plaques in Alzheimer’s
Alzheimers effects on cerebral cortex:
diffuse, sulci bw gyri are very wide, representing atrophy, ventricles dilated, loss of cortical neurons- almost 50%, neural connections to create memory, calculation and reasoning are lost, leads to dementia, senile plaques:
What are senile plaques in Alzheimer’s made of?
Core: amyloid, surrounded by degenerating neurites (damaged neurons)
Pathogenesis of Alzheimer’s – Amyloid
Several pws, all begin with Beta-amyloid deposits (plaques in brain), neurotoxic w loss of neurons (activates macs inducing inflammation, accelerates apoptosis of neurons)
Amyloid Formation and Breakdown:
APP (Amyloid Precursor Protein) formation, may be increased (Ex. Down’s Syndrome), cleavage/degradation may be reduced
APP:
normal membrane protein, 563-770 AAs
May lead to the reduction of amyloid breakdown:
Secretase enzymes break down APP, failure of breakdown → amyloid deposits
process of amyloid breakdown failure:
Alpha secretase cuts amyloid in half so that it becomes soluble and goes away, if alpha secretase doesn’t cleave, the amyloid is intact and insoluble, Beta and Gamma secretases then liberate the amyloid so that it floats free and deposits in the brain, may also have a mutation in alpha secretase that causes it to cleave the wrong area or not at all.
Parkinsonism:
Syndrome, not a single disease, 50-70yo, tremor at rest, rigidity, bradykinesia (slow movements), disorder of involuntary nervous system (normally modulates motor activity), gradually results in disability
Causes of parkinsonism:
Idiopathic: classical Parkinson’s disease, hereditary: alpha-synuclein gene, post-encephalitic: viral encephalitis, toxic: MPTP, cycad beans, pesticides?, head trauma
Loss of neuromelanin =
loss of neurons containing melanin
Parkinson’s Disease:
Cytoplasmic Lewy Bodies (dense center, lighter halo around), composed of filaments, contain alpha-synuclein, neurons with Lewy bodies are damaged and will die
Trigeminal Neuralgia is aka:
Tic douloureux
Trigeminal Neuralgia:
Sudden, severe, stabbing pain, many small attacks, lasting < 2m each (episodic), triggered by: touching face, brushing teeth, but mostly nothing
Causes of Trigeminal Neuralgia:
Usually idiopathic, vascular compression?, MS, tumors
Trigeminal Neuralgia presents similarly to:
neuralgia inducing osteonecrosis of jaw
pain is least common in the branch of CNV in Trigeminal neuralgia:
Division 1
Pathogenesis of Trigeminal neuralgia:
Nerve root compressed by vascular structure, irritation of nerve → hyperactive nerve nucleus, myelin begins to break down on CN V
Causes of Bell’s Palsy:
Idiopathic, trauma: surgery of parotid gland, infections: herpes simplex, zoster, Lyme disease, tumors, demyelinating diseases (MS, Guillain-Barré)
Bell’s Palsy:
Often subacute onset and course (Self-limited, 85% improve in 3wks), facial paralysis- usually unilateral (Eyelid can’t close, mouth droops), slurred speech, drooling, decreased lacrimation, taste
