Neuro Flashcards
pain sensitive cranial structures
scalp sinuses (periosteum) meninges pial arteries arteries and major veins
pain insensitive cranial structures
ventricles
choroid
brain parenchyma (except portion of midbrain)
small parenchymal and dural veins
vascular etiology of pain
distension/traction/dilation
traction or displacement of a larger caliber vein
nerve etiology of pain
traction or compression of a nerve
meningial etiology of pain
traction, displacement, irritation, inflammation of dura
muscular etiology of pain
abnormal contracture, spasm, irritation or inflammation of cranial or cervical musculature
brainstem etiology of pain
activation of area near dorsal raphe nucleus
induces migraine type pain
pathophysiology of migraine
abnormal instability or activation of cells which stimulate the trigeminal system
-causes stimulation of chemoreceptors and autonomic nervous system
diagnosis of common migraine
headache lasting 4-72 hours unilateral pulsating moderate or severe pain intensity aggravation or causing avoidance of physical activity nausea and/or vomiting photophobia and phonophobia
diagnosis of classic migraine
presence of aura-develops gradually over 5-20 minutes and lasts for less than 60 minutes
common auras-visual change, paresthesia, confusion
common visual auras
scintillating scotoma
central scotoma
diagnosis of basilar migraine
aura consisting of no motor weakness and dysarthria, vertigo, tinnitus, hypacusia, diplopia, visual symptoms in both temporal and nasal fields, ataxia, decreased consciousness, bilateral paresthesias
at least one aura gradually over 5 min (lasting no longer than 60 min)
common migraine triggers
red wine chocolate cheese MSG heavy nitrite containing food hunger from missing meals sleep deprivation irregular sleep patterns stress
migraine abortive pharmacology
NSAIDs-ibuprofen, naprosyn, ketorlac
5HT1 agonists-triptans and ergots
Dopamine antagonists-metoclopramide, prochlorperazine
prophylactic phrmacology for migraine
beta adrenergic blockers calcium channel blockers TCA anticonvulsants-gabapentin, valproic a cid, topiramate serotonergic drugs-cyproheptadine
most effective in children
cyproheptadine
serotonergic drugs
pathophysiology of cluster headaches
derived from hypothalamus
secondary activation of trigeminal-autonomic reflex
diagnosis of cluster headaches
episodic headache
attacks of severe unilateral stabbing periorbital or temporal pain
clusters for 3-6 weeks (at least 5 headaches lasting 15-180 min)
associated with autonomic symptoms (ipsilateal lacrimation, congestion, rhinorrhea, eyelid edema, facial sweating, miosis, ptosis)
abortive pharmacology of cluster headaches
oxygen-12L/min for 15 minutes most effective abortive agent
triptans-short onset (sumatriptan)
intranasal lidocaine
prophylactic pharmacology of cluster headaches
high dose steroids-prednisone
calcium channel blockers-adjuvant of choice
lithium
tension headache diagnosis
squeezing or pressure around head
may complain of light and sound sensitivity
never associated with nausea or vomiting
lasts 30 min-7 days
bilateral location
not aggravated by routine physical activity
non-pharmacological treatment of tension headaches
stress reduction
biofeedback
cognitive behavioral therapy
improved sleep hygiene
abortive therapy of tension headaches
acetaminophen
NSAIDs
Aspirin
prophylactic therapy of tension headaches
TCA
Antiepileptic-Gabapentin
pathophysiology of idiopathic intracranial hypertension
obstructive segments in the distal transverse sinus and presence of increased arterial inflow
stenosis of transverse sinus
obesity causes increase intra-abdominal pressure and increases cardiac filling pressures
symptoms of idiopathic intracranial hypertension
- nonspecific headache
- throbbing that worsens with valsalva
- pulsatile tinnitus-audible whooshing
- vision impairment-flashes and floaters, diplopia, decreased acuity and impaired visual fields, visual dimming with valsalva
- bilateral disc edema due to increased intracranial pressure
possible MRI findings for idiopathic intracranial hypertension
small slitlike ventricles
enlarged optic nerve sheaths
occasionally an empty sella
neuroimaging to rule out mass or dural venous sinus thrombosis
lumbar puncture in IIH
localize at L3-L4 (corresponds to superior iliac crest)
if obese, find sacral promontroy-L5-S1 interspace
CSF pressures
diagnosis of IIH >250mmH2O
normal pressure typically 120-170mmH2O
non-pharmacological treatment of IIH
diet
bariatric surgery
pharmacological treatment of IIH
diuretis-acetazolamide, furosemide
corticosteroid
anticonvulsants-topiramate (CA inhibitor, side effect is weight loss)
surgical indications for IIH
failed medical management -increased ICP -visual deterioration -worsening disc edema shunts-ventriculoperitoneal or lumboperitoneal
giant cell arteritis (temporal arteritis) pathophysiology
inflammatory response of internal elastic lamina
release of cytokines attracts macrophages and multinucleated giant cells
CD4T responsible for diseased vessel on histology
patchy manner
characteristics of temporal arteritis
headache-unilateral, temporal location
vision impairment-transient, intermittent
neck, torso, shoulder, and pelvic girdle pain consistent with polymyalgia rheumatic
fatigue and malaise
jaw claudication
mild fever
diagnosis of temporal arteritis
ESR and CRP elevated
temporal artery biopsy-large segment required
treatment of temporal arteritis
high dose steroids relieve headache within 3 days
most remain on low dose steroid for a couple of years
consequences of long term steroids
diabetes, vertebral compression fractures, steroid myopathy, steroid psychosis, immunosuppression
clinical presentation of brain tumors
increased ICP headaches, NV, CN3 and CN 6 palsy papilledema hemiparesis, aphasia, seizures tumors in ventricles present with hydrocephalus
diagnosis of brain tumors
MRI with contrast
BBB prevents contrast from entering healthy brain
leaky vessels allow tumor contrast to enter-contrast enhancing lesion
risk factor for brain tumors
ionizing radiation
characteristics of infiltrating astrocytoma
range from well differentiated to undifferentiated
can progress to glioblastoma with accumulation of mutations
grade I astrocytoma
pilocytic astrocytoma
grade II astrocytoma
diffuse or fibrillary astrocytoma
grade III astrocytoma
anaplastic astrocytoma
grade IV astrocytoma
glioblastoma
presentation of diffuse astrocytoma
younger patients
seizure, HA, focal neurologic deficits
median survival 5 years
histology of diffuse astrocytoma
increase in glial cells
GFAP positive
histology of anaplastic astrocytoma
more densely cellular
greater nuclear pleomorphism
mitotic figures
diagnosis of diffuse and anaplastic astrocytoma
non-enhancing lesion
may not be seen on CT
treatment of diffuse and anaplastic astrocytoma
surgical resection
often cannot be resected due to size and location
radiation-most effective nonsurgical treatment
primary vs secondary glioblastoma
primary-most common, onset in older people
secondary-younger patients, due to progression of lower grade astrocytoma
classic glioblastoma genetics
PTEN mutations
deletion of chromosome 10
most common primary
genetics proneural glioblastoma
TP53
point mutations in IDH1 and IDH2
most common secondary
genetics mesenchymal glioblastoma
deletions or lower expression of NF1 on chromosome 17
histology glioblastoma
densely cellular
necrosis
vascular proliferation
pseudopalisading
diagnosis and treatment glioblastoma
MRI-ring enhancing lesion
surgery, radiation, chemotherapy
mean survival 15 months
characteristics of pliocytic astrocytoma
children and young adults
often cystic with mural nodule in wall of cyst
grows slowly, recurrence involves cyst enlargement rather than growth of solid component
locations of pliocytic astrocytoma
cerebellum
third ventricle
histology of pliocytic astrocytoma
cells with hair-like processes
Rosenthal fibers from long standing gliosis
characteristics of oligodendroglioma
adults in 40-50
slow growing
in cerebral hemispheres
calcifications!
histology of oligodendroglioma
sheets of regular cells with spherical nuclei, surrounded by clear halo of cytoplasm (poached egg appearance)
genetics of oligodendroglioma
mutations in IDH1 and IDH2
deletions in chromosome 1p and 19q
treatment of oligodendroglioma
surgery, radiation, chemotherapy
characteristics of ependymoma
tumor of children and young adults
occur in ependymal lined ventricular system
locations of ependymoma
adults-spinal cord
children and young adults-fourth ventricle
presentation of ependymoma
hydrocephalus
CSF dissemination
histology of ependymoma
small dark cells, variably dense fibrillary background between nuclei, form perivascualr pseudorosettes, benign appearing
genetics of ependymoma
spinal cord-NF2 mutation chromosome 22