Neuro Five Flashcards
MS signs
Motor and sensory from spinal cord
Ataxia and nystagmus
Frequency of relapses decrease during course but steady neurologic deterioration
Central pontine myeloysis
Symmetric demyelination
Myelin loss no inflammation
Parkinson histo
Loss of pigmentation substantia nigra
Lewy body
ALS time
Fifty or older
SODone is on chromosome twenty one get gain of function alanine to valine
Btwelve defiency
Anemia
Or neurologic which presents a few weeks as numbness, tingling, slight ataxia in LE
Rapid progression:spastic weakness of LE
Complete paraplegia
Replacement can improve unless complete paraplegia has developed
Histo Btwelve defiency
Swelling of myelin layers make vacuoles
Axons of ascending and descending tracts degenerate
SuBACute combined degeneration of SPC spinal cord
Axons of both are degenerated
Corneal stroma
No blood vessels or lymphatics
Why get corneal vasculrization
Chronic corneal edema
Inflammation scarring
Risk factor glaucoma
DM
Cytotoxic edema can lead to
Hernation
Vasogenic edema follows what
Ischemic injury
Thrombosis is mainly due to
Atherosclerosis
Rupture , ulceration or erosion of plaque exposes blood to thrombogenic substance get clot
Tia transient ischemic attack
One hour smal infarct One day function lost Neurologic emergency Fifteen perfect have a stroke causes persistent deficits within three months, Half within first forty eight hours
MOA embolus temporarily occluded then dissolves , get thrombosis formation or vasoaspasm
Hypertension and brain
Lacune
Slit hemorrhages
Hypertensive encephalopathy
-deep brain
Vascular multi infarct dementia-dementia gait and pseudobulbar signs
Binswanger disease-large area of subcortical white matter with myelin and axon loss
Charcot Bouchard-microaneurysms associate with chronic HTN
Bacterial meningitis complication
Seizure, encephalitis, hearing loss, blindness, paralysis
Fulminant with meningococcemia, rash
Adrenal hemorrhage->death
Waterhouse friderichsen syndrome
Bacterial meningitis
Pressure over 10 Cloudy turbid Neutrophils over 100 Lymph over 5 ml Glucose less than 50 Protein 50-1000
Virus meningitis
Clear colorless, no neutrophils, lymph mono 0-5
Glucose 50-80
Protein 15-45
Neisseria meningitidis
Epidemiology
Colonized the oropharynx and rhinopharynx of asymptomatic carriers and spreads by direct contact with respiratoy secretions
Higher in crowded populations like dorms prisons
N meningitidis clinical manifestations
Rapidly progressive septicemia with fever, hypotension DIC, petechial and purpuric lesions
Purpura fulimans:hemorrhagic skin lesions which progress to gangrene;occurs in distal portions of limbs
Hemorrhagic infarction of adrenal glands
Chronic meningitis symptoms
Fever, headache, lethargy, confusion, nausea, vomiting, stiff neck
CSF chronic meningitis
Elevated protein concentration, predominantly lymphocytic pleocytosis, sometimes a low glucose level
TB, neuroborreliosis, neurosyphilis
Diagnose chronic meningitis
Diagnosis is made if symptoms and CSF persist or progress for a period of at least 4 weeks
Treponema pallidus
Neurosyphilis
Meningovascular neurosyphilis
Paretic neurosyphilis
Tabes dorsalis
Neurosyphilis
Tertiary stage: only about 10% of untreated PTs develop
Meningovascular neurosyphilis
Chronic meningitis involving base of the brain (variable convexities and spinal leptomeninges)
Paretic neurosyphilis
Insidious but progressive mental deficits associated with mood alterations (delusions of gradeur0 that terminate in severe dementia (general paresis of the insane ) perivascular iron deposits
Granular ependymomas:proliferation of subependymal glia under damaged ependymal linings associated with hydrocephalus
Tables dorsalis
Damage to the sensory nerves (loss of myelin and axons) in the dorsal roots; impaired joint position sense and resultant ataxia (locomotor ataxia);loss of pain sensation (Charcot joints) lightening pains;absence of DTR
Herpes
Chickenpox cutaneous
Latent phase:in sensory neurons of dorsal root or trigeminal ganglia
Reactivation(shingles) painful ) vesicular skin eruption limited to a single or limited dermatome
Persistent postherpetic neuralgia syndrome:perstent pain as well as painful sensation following nonpainful stimuli
Rabies
Incubation period 1-3 months depends on distance of wound to the brain
Infection ascends along peripheral nerves fromt he wound site
Nonspecific symptoms (malaise HA, fever) with local paresthesia around wound (diagnostic)
Extraordinary CNS excitability;violent motor responses progressing to convulsions
Flaccid paralysis , respiratoy center failure
Hydrophobia dopamine at the mouth due to contracture of pharyngeal muscles that produce an aversion to swallowing
CJD
90% prion seventh decade
Iatrogenic transmission:corneal transplant, brain implant or electrodes and HGH
Rapidly progressice dementia with startle myoclonus 7 months
So rapid , little if any gross evidence of brain atrophy (spongiform changes microscopic)
VCJD
UK young adults
Behavioral changes early in DZ
Slower progression
Exposure to bovine spongiform encephalopathy
Kuru plaque : extracellular deposits of aggregated ABN protein +Congo red and +PAS
Cerebellum of VCJD
FFI fatal familial insomnia
Sleep disturbances initially less than three year survival
Aspartate substitution at 129
Ataxia, autonomic disturbances, stupor and coma
Most cases of AD are
Sporadic@
5-10% familial
Pathological examination necessary for definitive diagnosis
Treat parkinson
L DOPA replaced with Carbidopa
Huntington
4p16.3
CAG normal 10-36 get adult onset with 40-50
Juvenile over 60
ALS early sign
Drop objects muscle strength and bulk dismissed
Fasciculations ALS
Involuntary muscle contraction
Respiratoy infections ALS
Respiratoy muscle involved
Progressive Muscl atrophy
LMN
Progressive bulbar palsy
Lower brainstem and cranial motor nuclei early and prognosis rapidly
2 year dead
ALS
2 year dead
Pilocytic astrocytoma
First two decades of life
Cerebral hemispheres or cerebellumNF1 predisposes, espicially optic tumors
Functional loss of neurofibromin in tumor
Well circumscribed often cystic with a ural nodule
Radiology discrete, contrast enhancement, lack or surrounding edema, cyst
Pilocytic astrocytoma
Biphasic pattern:loose glial with cystic changes and dense piloted. Tissue
Hair like cells with long bipolar processes
Rosenthal fibers
Eosinophilia granular bodies (EGBs)
Extension into subarachnoid space is common (not sign of aggressiveness) espicially with optic nerve lesions
GFAP positive
Glioblastoma (IV/IV)
Most common primary brain neoplasm
Primary vs secondary neoplasms
Primary-later in like (older patient, no precursor lesion (EGFR and PTEN)
Secondary-preceded by lower grade lesions (TP53), IDH1 (R132 H mutation has better prognosis) and IDH2 typically younger
Throughout brain
Contrast ring enhancing hypodense central necrosisi
Cells follow fiber tracts and extend well beyond imaging
Glioblastoma histology
Necrosis : serpentine pattern of necrosis in hypercellular areas
Pseudo-palisading of cells around necrosis
Vascular/endothelial proliferation
- VEGF produced by malignant astrocytes in response to hypoxia is responsible
- tufts of cells pile up and bulge into vascular lumen
- glomeruloid body: MKD proliferation produces a ball like structure
Oligodendroglioma
10-15% of all gliomas, primarily adults
Primary cerebral hemispheres
Calcification usually restricted to the cortex, curving around or gyriform distribution
Histology:perineuronal satellitosis, perivascular aggregation and subpial accumulation of tumor cells
Perinuclear halos fried eggs
Delicate anastomsing capillaries chicken wire
Most are well differentiate grade II, IV
IDH1 and IDH2 isocitrates dehydrogenase genes, most common mutation in oligodendrocytes (90%) favorable prognosis
1p19q loss favorable prognosis
Anaplastic oligo II/Iv-vascular hypertrophy and necrosis, often retains geometric vascularity often retains geometric vascularity
Increased grease with increased N;C, mitosis and cellularity
Often these features found in nodules located within a IIIV tumor
Poor prognosis similar to glioblastoma
Four molecular groups
Malignant embryonal tumor in children (20% of brain tumors in kids)
- 4 molecular GRPS
- WNT: older kids, monosomy CHR 6, B catenin, 5 YR survival 90%
- SHH: sonic hedgehog, infants-young adults, nodular desmoplastic morph, MYCN AMP, prognosis intermediate between WNT and GRPS 3 and4)
Group 3:MYC AMP 17(i17Q) infants, kids-classic or LG cell, worst prognosis
Group 4 17Q, NO MYC or MYCN, intermediate, 17Q poor prognosis, classic or LG cell morphology