Neuro Flashcards
Middle Cerebral Artery Stroke: Signs / Sx etc.
contralateral hemiparesis + hemisensory loss of the FACE and UPPER LIMB
other features = anosognosia (insight lack), contralateral spatial neglect (if in non-dominant parietal lobe), conjugate gaze deviation TOWARD lesion side, contralateral homonymous hemianopsia (optic radiation damage in subcortical temporoparietal)
Anterior Cerebral Artery Stroke: Signs / Sx etc.
contralateral hemiparesis of LOWER limb
if bilateral ACA occlusion, may have ABULIA (lack of initiative/will), primitive reflexes (Moro, grasp), urinary incontinence (prefrontal cortex damage)
Posterior Cerebral Artery Stroke: Signs/ Sx etc.
contralateral hemianopia with macular sparing (due to collateral circ. from MCA) via visual cortex infarction
Basilar Artery Occlusion: Signs/ Sx etc.
damages corticospinal / -bulbar tracts
quadriplegia; bulbar dysfunction (facial weakness, dysarthria) and oculomotor issues (horizontal gaze palsy)
Anterior Inferior Cerebellar Artery occlusion: Signs / sx etc.
LATERAL PONTINE SYNDROME
ipsilateral pain/temp loss (trigeminal nucleus)
ipsi facial weakness (facial nucleus)
ipsi hearing loss (cochlear nucleus)
contra pain/temp trunk/limbs (lateral spinothalamic)
cerebellar dysfunction (ataxia, dysmetria)
Anterior Communicating Artery aneurysm: signs sx etc
compresses central optic chiasm
bitemporal hemianopia
Posterior Communicating Artery aneurysm: signs sx etc.
compresses CN III
ipsilateral mydriasis, ptosis + “down n out” deviation
Histopathology of brain biopsy shows:
amyloid deposits in cortical vessels
what’s the condition?
cerebral amyloid angiopathy
beta amyloid; usually asymptomatic, can be assoc. with hemorrhage or Alzheimer’s dementia
Histopatho of brain shows:
Congo red staining plaques in hippocampus
what’s the condition?
Alzheimer’s
neuritic (senile) plaques of EC beta amyloid surround dystrophic neurites (Congo+ and often hippocampal)
Histopatho of brain shows:
Eosinophilic, round cytoplasmic neuronal inclusions
what’s the condition?
Rabies
Negri bodies, especially in Purkinje and hippocampal pyramidal cells
Histopatho of brain shows:
profound neuronal loss in caudate nucleus
what’s the condition?
Huntington disease (AD)
choreiform movement, psych disturbance, dementia
Histopatho of brain shows:
Slit-like white matter cavities with surrounding gliosis
what’s the condition?
Lacunar infarction
recurrent in vascular dementia, with stepwise cognitive decline + focal deficits (older pt with CV risk factors such as DM and htn)
Histopatho of brain shows:
Microglial nodules and multinucleated giant cells
what’s the condition?
HIV-associated dementia
HIV enters CNS via infected macrophages and infects microglia > subcortical dementia with memory deficits, executive dysfunction + slow info processing
CD4 < 200/mm3
Meningioma: histo, signs / sx, etc.
slow-growing benign tumor of arachnoid meningothelium
“whorled” cell pattern of syncytial nests; psammoma bodies
well-circ round mass attached to dura at falcine, parasagittal, tentorial or lateral brain convexities
s/s are seizure via compression; HA/nausea/vom via ICP (worse lying or sleeping); focal neuro deficits by size/location
Ependymoma: epidemiology, histo, site
10% of posterior fossa tumors in kids
histo = characteristic perivascular rosettes (pink fibrous material around vessel); GFAP+ processes tapering towards vessels
paraventricular tumors in kids (eg, floor of fourth ventricle, other sites of ependymal cells); spinal ependymomas in adults
Glioblastoma: histo, morpho, site, epidemiology
1 primary malignant brain tumor of adults (40-70)
soft + poorly defined; can be very large –> mass effects and midline shift; areas of necrosis + hemorrhage with microvascular prolif.
seen in cerebral hemispheres (frontal, temporal, basal ganglia) + may cross corpus callosum with “butterfly glioma” appearance on img
histo = hypercellular areas of atypical astrocytes that border regions of necrosis (“pseudo-palisading”); poorly diff, pleomorphic astrocytes; nuclear atypia + many mitoses
Medulloblastoma: epidemiology + histo
malignant cerebellar tumors in children
small blue cells (primitive neuroectodermal tumor, PNET) with high mitotic index
Homer-Wright rosettes (cells surround neuropil) in 20%
Oligodendroglioma: site, morpho + histo
white matter of cerebral hemispheres; well-circumscribed gray mass with calcification
“fried egg” cells (round nucleus + halo of clear cytoplasm)
Pilocytic Astrocytoma: epidemiology; site; histo
usually benign in cerebellum (or brainstem, hypothalamus, optic path) of kids / young adults
histo = eosinophilic granular bodies and elongated hairlike processes (Rosenthal fibers: pink fibrous material); well-diff with spindle cells + hair-like glial processes + microcysts
Schwannoma: site, histo
mostly benign; vestibular branch of CN VIII at cerebellopontine angle
histo = spindle cells with palisading nuclei around “Verocay bodies” with an eosinophilic core (Antoni A pattern)
Craniopharyngioma: epidemiology, site, histo
benign suprasellar tumor in kids
cords/nests of palisading squamous epithelium with internal areas of lamellar “wet keratin”
Primary CNS Lymphoma: epidemiology, morpho
immunocompromised (HIV, transplant) pts; in HIV can be via EBV infection
multiple lesions in deep grey matter, white matter + cortex
Brain metastases: morphology / imaging, common primary tumor sites
lung, breast, kidney and skin (melanoma)
typically multiple, well-circ masses at grey-white matter junction
Neuroblastoma:
site, epidem, histo + markers
mutation
1 extracranial solid tumor in kids
small, round, blue cell tumors; “neuropil” (neuritic process pathognomonic of neuroblastoma cells)
NSE, chromogranin, synaptophysin and S-100 positive on IHC
urinary HVA and/or VMA high in 90%
N-MYC (chr. 2) is mutated
Pituitary Apoplexy: etiology, s/s, dx and tx
how to diff from aneurysm rupture near optic chiasm?
acute pituitary hemorrhage assoc. with pituitary adenoma
sudden severe HA bitemporal hemianopsia ophthalmoplegia (CN III) hemodynamic instability (low cortisol) altered sensorium antecedent loss of libido (high PRL) chronic mild HAs
dx by CT or MRI
tx by surgery and steroids
diff from saccular aneurysm rupture by history of pituitary dysfunction prior to acute event + CV collapse during event
Basal ganglia hemorrhage: etiology, s/s
usually via chronic hypertensive vasculopathy
neuro deficits that gradually worsen over minutes - hrs
contralateral hemiparesis, hemianesthesia (corticospinal + somatosensory tract disruption)
Carotid dissection: etiology, s/s
trauma, chronic htn, CT disease or smoking can cause
unilateral HA, transient vision loss, ptosis + miosis (partial Horner syn.)
Cerebral venous sinus thrombosis: etiology, s/s
thrombophilia, pregnancy, contraceptives, malignancy or infection can cause
presents with HA, vomiting, seizure and focal neuro deficits
anoxic brain injury MRI findings
loss of grey-white matter differentiation
sulcal effacement
(common in cardiac arrest)
pupillary reflex pathway
retina > optic nerve > superior colliculus-level midbrain > pretectal nucleus > BILATERAL Edinger-Westphal nuclei > oculomotor nerve (preganglionic PSNS) > ciliary ganglion > postganglionic fibers to sphincter pupillae
Epidural hematoma: vessel, location, clinical s/s, CT
middle meningeal artery; btwn skull + dura
lucid interval, followed by loss of consciousness
biconvex hematoma on CT
Subdural hematoma: vessel, location, clinical s/s, CT
bridging cortical veins; btwn dura + arachnoid
gradual onset HA/confusion
crescent shaped hematoma on CT
SAH hematoma: vessel, location, clinical s/s, CT
ruptured aneurysm/AV malformation of ant/post communicating arteries or MCA; btwn arachnoid + pia
sudden severe headache, fever, NUCHAL RIGIDITY (develops within 24 hrs as blood irritates meninges)
may see PAPILLEDEMA or PUPILLARY DILATION (but no focal neuro deficits)
blood in basal cisterns on CT
L2 radiculopathy: sensory + motor sx
upper anteromedial thigh
weak hip flexion (iliopsoas)
L3 radiculopathy: sensory + motor sx
lower anteromedial thigh
weak hip flexion (iliopsoas), hip adduction, knee extension (quad)
L4 radiculopathy: sensory + motor sx
lower anterolateral thigh, knee, medial calf + foot
weak hip adduction, knee extension (quad) and PATELLAR reflex
L5 radiculopathy: sensory + motor sx
buttocks, posterolateral thigh, anterolateral leg, dorsal foot
weak foot dorsiflexion + inversion (tibialis anterior), foot eversion (peroneus), and toe extension (extensor hallucis + digitorum)
S1 radiculopathy: sensory + motor sx
buttocks, posterior thigh + calf, lateral foot
weak hip extension (glut max), knee flexion (hamstrings), foot plantarflexion (gastroc) and ACHILLES reflex
Babinski sign
what does it indicate, how is it done, associated sx
stroke sole from lateral heel to ball of foot
dorsiflexion with toe spreading is positive in adults + indicates UPPER MOTOR NEURON LESION
assoc. findings are spasticity, hyperreflexia, muscle weakness/paralysis
(dorsiflexion normal in babies due to incomplete myelination of corticospinal tracts)
Acute cerebellitis
AKA? epidemiology + causes? Sx and course?
aka post-viral cerebellar ataxia
children 2-3 wks old via varicella, measles, or EBV
ataxia, nystagmus + dysarthria; usually resolves by 3 weeks
Cerebellar Infarction
presentation? biopsy/autopsy findings?
vertigo, nystagmus, IPSILATERAL limb ataxia, and TRUNCAL LATEROPULSION (fall toward lesion)
autopsy shows liquefactive necrosis (acute infarct) and glial scarring (chronic infarct)
Opsoclonus-Myoclonus syndrome
s/s, association
nonrhythmic conjugate eye movements, involuntary limb + trunk jerking
rare paraneoplastic condition from NEUROBLASTOMA (thought to be via an auto-ab)
(N-myc, SRB cells, Homer-Wright rosettes and urinary HVA/VMA)
Hypothalamic nuclei functions:
ventromedial, lateral, anterior, posterior
ventromedial - monitors blood glucose; mediates SATIETY; lesions cause HYPERPHAGIA
lateral - mediates HUNGER; lesions cause ANOREXIA
anterior - mediates heat dissipation; lesions cause HYPERthermia
posterior - mediates heat conservation; lesions cause HYPOthermia
Hypothalamic nuclei functions:
arcuate
paraventricular
supraoptic
suprachiasmatic
arcuate - secretes dopamine (inhibits PRL), GHRH and GnRH
paraventricular - ADH, CRH, oxytocin + TRH secretion
supraoptic - ADH + oxytocin secretion
suprachiasmatic - circadian rhythm + pineal gland function
Tumors of hypothalamus
most common in kids? most common in adults?
gliomas in kids
metastases in adults
Cavernous Hemangioma in CNS
where? s/s? complications?
in brain parenchyma ABOVE TENTORIUM CEREBELLI
seizures + progressive neuro deficits due to mass effects
tend to bleed > intracerebral hemorrhage
Transtentorial Herniation
what is it? cause?
ocular sx?
herniation of the medial-most portion of the temporal lobe (uncus) around/below the tentorium cerebelli
large cerebral hemorrhages, tumors etc. with mass effects can cause it
ipsilateral CN III disruption > ipsilateral fixed DILATED pupil with “DOWN AND OUT” deviation
herniation progression > midbrain + upper pons injury causes MID-POSITION and fixed pupil BILATERALLY w/ loss of vestibulo-ocular reflex
Decerebrate Posturing
what is it? what causes it?
EXTENSOR posturing via loss of RUBROSPINAL descending upper limb flexor excitation and unopposed VESTIBULOSPINAL extensor output
BRAINSTEM damage AT/BELOW RED NUCLEUS (midbrain tegmentum / pons)
Decorticate posturing
what is it? what causes it?
FLEXOR posturing due to loss of DESCENDING INHIBITION of the red nucleus (upper limb flexion)
damage to structures ABOVE RED NUCLEUS such as CEREBRAL HEMISPHERES or INTERNAL CAPSULE
Cerebellar vermis damage
signs?
vermis controls AXIAL/PROXIMAL LIMB muscle coordination
damage causes GAIT / TRUNCAL ATAXIA; may also cause nystagmus/vertigo via role in vestibular function
Thalamus damage
signs?
thalamus is relay station for almost all ascending sensory info
damage > sensory loss; bilateral damage may cause coma
Multiple Sclerosis
signs + symptoms
sx are EPISODIC + PROGRESSIVE
sensory disturbance; motor weakness; bowel/bladder issues
ocular issues: OPTIC NEURITIS (painful movement, intermittent vision decrease, optic disc swelling); INTERNUCLEAR OPHTHALMOPLEGIA (impaired adduction on lateral gaze)
cerebellar dysfunction: INTENTION TREMOR and BROAD GAIT
LHERMITTE SIGN: electrical sensation in limbs/back with neck flexion
UHTHOFF PHENOMENON: sx worse with increased body temp (slow conduction in damaged nerves)
Multiple Sclerosis
risk factors (race, gender, genetics, environment)
white females
HLA-DRB1
US / Europe; colder climates
low vitamin D and smoking
Multiple Sclerosis
diagnosis (clinical, imaging, other)
episodic/progressive sx disseminated over time/space
MRI shows HYPERINTENSE T2 lesions (demyelinating plaques)
CSF shows OLIGOCLONAL IgG bands
Wallenberg syndrome
cause? s/s?
LATERAL MEDULLA lesion - affects pain/temp tracts plus CN V 5, 9, 10 and 11
vertigo/nystagmus; ipsilateral ataxia + dysmetria (cerebellar)
loss of pain/temp in IPSILATERAL FACE + CONTRALATERAL BODY
bulbar weakness (dysphagia)
ipsilateral Horner
Colloid cyst
what? where? histo? complications?
BENIGN cyst in THIRD VENTRICLE
rare mitoses
lethal obstructive hydrocephalus
Pleomorphic Xanthoastrocytoma
what? in whom? histo? progression?
astrocytoma in KIDS / YOUNG ADULTS
RETICULIN deposits and CHRONIC WBC INFILTRATES
may progress to glioblastoma multiforme (rarely)
What is Wallerian degeneration?
How does it occur in CNS? Timeline?
axon damage > axon degeneration + myelin sheath breakdown DISTAL TO INJURY (begins few days after lesion)
in CNS, occurs more slowly due to BBB
macros/microglia enter more slowly > MYELIN DEBRIS PERSISTS FOR YEARS causing slower axonal growth
GLIAL SCAR in weeks/months after injury also slows process
Substructures + sheathing of nerves
Nerve is surrounded by EPINEURIUM and made up of FASCICLES (bundles of axons) surrounded by PERINEURIUM
Each axon is surrounded by an ENDONEURIUM
Guillain Barre histo
ENDONEURIAL inflammation
perivenular lymphos and macros btwn vessel and its assoc. axon
macros may appear LIPID LADEN after engulfing myelin
1 diagnosed movement disorder
cause? s/s? tx?
Essential tremor
(aka familial tremor, sometimes follows AD inheritance)
worsens while maintaining a certain posture (eg, holding an object)
improves with alcohol consumption
PROPRANOLOL is first-line
Thalamus VPL nucleus
inputs from where? what sensations?
contralateral…
spinothalamic tract - touch, pain, temp
dorsal columns - vibration + proprioception
Thalamus VPM nucleus
inputs from where?
trigeminal pathway
touch and pain in face
Lacunar infarct
affects what structures? what vessels?
basal ganglia, posterior limb internal capsule, pons + cerebellum
small penetrating arteries (eg, lenticulostriate)
Lacunar infarct
causes?
pathogenesis / histo (2 main features)?
uncontrolled HYPERTENSION and DIABETES
LIPOHYALINOSIS - leakage of plasma proteins > hyaline vessel thickening, sclerosis and foamy macros
MICROATHEROMAS - foamy macros accumulate near origin of penetrating vessel
Liquefactive necrosis > small cavitary infarct
Amyotrophic Lateral Sclerosis
in whom? MC-COD?
what tracts / areas damaged?
middle-aged pt
COD = respiratory complications (aspiration pneumonia)
affects ANTERIOR HORNS (lmn lesion) and LATERAL CORTICOSPINAL TRACTS (umn lesion)
also MOTOR nuclei of CN V, IX, X, XII
Amyotrophic Lateral Sclerosis
mutation? histo of muscle? tx?
SOD1 mutation - codes for copper-zinc superoxide dismutase
muscle shows DENERVATION ATROPHY with SMALL, ANGULAR FIBERS
Riluzole - decreases Glu release
Neurofibromatosis Type I
inheritance + gene? two skin manifestations and their origin?
von Recklinghausen disease; AD inherited mutation of NF1 tumor suppressor
Cafe-Au-Lait Spots - hyperpigmented macules of the trunk (melanocytes); soon after birth
Cutaneous neurofibromas - early adolescence; multiple raised tumors; grow and multiply with age (< 2cm); from Schwann cells
all from neural crest cells
NF type I
risk of what?
CNS neoplasms such as OPTIC GLIOMA and PILOCYTIC ASTROCYTOMA
Oculomotor Palsy
causes? s/s?
tumors, aneurysms (specif. POST. COMMUNICATING A.)
nerve ischemia, trauma
ptosis (levator palpebrae) DIAGONAL DIPLOPIA impaired adduction (medial rectus) impaired depression (inferior rectus) impaired elevation (superior rectus) impaired constriction + accommodation
causes a DOWN AND OUT deviation, via unopposed lateral rectus and superior oblique action
Trochlear palsy
s/s?
SUPERIOR OBLIQUE function is disturbed (poor abduction, internal rotation + depression when adducted)
eye deviates UPWARD
vertical + torsional diplopia
Abducens palsy
s/s?
LATERAL RECTUS function disturbed (poor abduction)
eye deviates MEDIALLY > HORIZONTAL diplopia
Trigeminal Neuralgia
s/s? trigger? duration?
tx?
stabbing/electric pain in CN V (esp. V/2 and V/3) distribution, usually UNILATERAL
lasts only SECONDS but REPEATEDLY and episodes can occur for months
trigger is any CN V stimulus: chewing, toothbrushing, shaving, washing face, swallowing, hot/cold
CARBAMAZEPINE is tx
(aplastic anemia / CYP induction >monitor CBCs and other drug levels)
Wernicke encephalopathy
s/s? iatrogenic cause?
ataxia, nystagmus, ophthalmoplegia, anterograde amnesia
IV dextrose without thiamine in chronic alcoholic with low thiamine at baseline
(dextrose precipitates use of all available thiamine and then a severe thiamine defic.)
Korsakoff psychosis
cause? brain area damaged? s/s?
(other brain area that MAY be affected, but not always)
CHRONIC thiamine defic. > MAMMILLARY BODY necrosis
antero-/retrograde amnesia, apathy, lack of insight, confabulation
(anterior nucleus of thalamus… also part of Papez circuit like mammillary bodies, can be affected)
Locus Ceruleus
Creates what? Involved in what? Injured by what?
Norepinephrine
involved in RETICULAR ACTIVATING SYSTEM (arousal), mood, sleep-wake states, cognition, BP control
dysfunction in ANXIETY DISORDERS (panic attacks, etc.)
BILATERAL PONTINE HEMORRHAGE - causes coma due to reticular activating system damage; also paralysis with EXTENSOR posturing (corticospinal/bulbar tract injury) and PINPOINT PUPILS
Transtentorial Herniation (aka uncal)
what can be compressed / occur? (4)
- OCULOMOTOR NERVE - ispilateral; first pupil is fixed and dilated, then muscles are paralyzed and a ptosis and “down and out” position occurs (sup. oblique + lateral rectus still function)
- POSTERIOR CEREBRAL ARTERY - ipsilateral artery > contralateral homonymous hemianopsia w/ macular sparing
- CONTRALATERAL CEREBRAL PEDUNCLE - damage to contralateral corticospinal tract > ipsilateral hemiparesis
- BASILAR ARTERY - can be stretched/ruptured causing brainstem (Duret) hemorrhage in pons/midbrain; often fatal
Subfalcine herniation
cause? result?
subdural hematoma causes cingulate gyrus to compress under falx cerebri
can compress ANTERIOR CEREBRAL ARTERY
Hemiballism
cause? structure affected? s/s?
LACUNAR STROKE (long-standing DM or htn) damamges the SUBTHALAMIC NUCLEUS, which no longer excites the globus pallidus internus > no longer inhibits the thalamus
wild, involuntary, large amplitude flinging movements of proximal limbs on ONE SIDE OF BODY (hemi-)
diff dx of hemiballism and Huntington’s motor issues
hemiballism - large amplitude movements of proximal limbs (subthalamic nucleus)
Huntington - low amplitude movements of distal limbs (caudate nucleus) plus dementia + behavioral issues
internal capsule damage
via what? what deficits?
lacunar infarct, tumor, etc.
contralateral pure motor or sensorimotor deficit
Wilson’s disease
affects what part of brain?
Lentiform nucleus (GP and putamen)
so-called “hepatolenticular degeneration” bc liver involved too
depression + personality changes
dysarthria and movement disorders
glossopharyngeal nerve functions
somatic motor?
PSNS?
general sensory?
special sensory?
somatic motor - STYLOPHARYNGEUS, elevates larynx on swallowing
psns - PAROTID SECRETION
general sensory - inner tympanic membrane, eustachian tube, post 1/3 tongue, tonsils, upper pharynx (gag!), carotid body + sinus
special sensory - post 1/3 tongue taste
what is the path for innervation of the parotid?
5 steps
- INFERIOR SALIVATORY NUCLEUS (inf. dorsal pons)
- travels along CN IX (glossophar.)
- OTIC GANGLION (infratemp fossa)
- AURICULOTEMPORAL n. (CN V/3)
- parotid gland
What are the 5 seizure types?
2 major categories plus subtypes
- FOCAL - 1 hemisphere at onset
- Simple - no loss of consciousness
- Complex - loss of consc. + POST-ICTAL state - GENERALIZED - both hemispheres at onset
- Tonic-clonic - lost consc., contraction + jerking
- Myoclonic - no lost consc. brief jerking
- Absence - brief consc. loss + automatisms
How is epilepsy treatment divided?
3 divisions
FOCAL seizures can be tx with NARROW SPECTRUM drugs (even if they evolve into tonic-clonic after onset!)
GENERALIZED seizures can be tx with BROAD SPECTRUM DRUGS
ABSENCE seizures are tx with ETHOSUXIMIDE
Pineal gland mass
common s/s?
(2 main syndromes plus 3 s/s for one and 3 s/s for the other)
OBSTRUCTIVE HYDROCEPHALUS - via aqueductal stenosis; causes 1) papilledema, 2) HA worse when lying 3) vomiting, usually in morning
DORSAL MIDBRAIN (Parinaud) SYNDROME - compression of pretectal midbrain; causes 1) limited upward gaze, 2) bilateral eyelid retraction (Collier sign), 3) light-near dissociation (accommodation without pupillary constriction)
What is the #1 pineal gland mass?
where else might it show up? in whom?
GERMINOMA - midline malignant tumor of embryonic germ cells
can also be suprasellar, gonad or mediastinum
more common in YOUNG BOYS
(causes obstructive hydrocephalus and Parinaud syndrome = downward gaze, eyelid retraction and light-near dissociation = pupils accommodate but don’t react to light)
What is “locked in” syndrome + what can cause it?
spastic quadriplegia (extensor posturing) and paralysis of most cranial nerves but PRESERVED CONSCIOUSNESS + EYE MOVEMENTS
via pontine hemorrhage or tumors
what do medial medulla lesions cause?
3 things
MEDIAL MEDULLARY SYNDROME
- contralateral SPASTIC PARALYSIS (umn lesion)
- contralateral VIBRATION/PROPRIO loss (dorsal columns)
- ipsilateral FLACCID TONGUE PARALYSIS (CN XII)
Charcot-Bouchard vs. Berry aneurysm
assoc. conditions
location
Charcot-Bouchard - ONLY via HYPERTENSION; found in basal ganglia (mostly PUTAMEN), thalamus, cerebellum + pons
Berry - via PCKD, Ehlers-Danlos and hypertension; in the CIRCLE OF WILLIS
Charcot-Bouchard vs. Berry aneurysm
size, result of rupture + s/s
Charcot-Bouchard - smaller (<1 mm); cause INTRACEREBRAL hemorrhage with PROGRESSIVE FOCAL DEFICITS +/- headache
Berry - variable (2-25 mm); cause SUBARACHNOID hemorrhage; sudden SEVERE HA without focal neuro sx
anterior 2/3 of internal capsule carries what?
posterior 1/3?
internal capsule lesions cause what?
anterior 2/3 - motor fibers (corticospinal tract)
posterior 1/3 - sensory fibers (thalamocortical tracts)
most lesions are CONTRALATERAL PURE MOTOR or SENSORIMOTOR (it would take a very small lesion to the posterior only to produce a pure sensory lesion)
What is INTERNUCLEAR OPHTHALMOPLEGIA?
what two nuclei + which tract are involved?
a disorder of CONJUGATE HORIZONTAL GAZE movements
communication between the ABDUCENS NUCLEUS (dorsal pons) and the contralateral OCULOMOTOR NUCLEUS (dorsal midbrain) via the MEDIAL LONGITUDINAL FASCICULUS is disrupted
Explain how CONJUGATE HORIZONTAL EYE MOVEMENT works
tracts + nuclei
- FRONTAL EYE FIELD - in frontal cortex, goes to…
- contralateral PARAMEDIAN PONTINE RETICULAR FORMATION, sends efferents to…
- ipsilateral ABDUCENS NUCLEUS (dorsal pons) to abduct ipsilateral eye, which sends efferents to…
- contralateral OCULOMOTOR NUCLEUS (dorsal midbrain) via MLF to adduct the contralateral eye
3 sx of internuclear ophthalmoplegia
what 2 things are preserved?
- IMPAIRED CONJUGATE HORIZONTAL GAZE - eye opposite the gaze can not adduct to look in the same direction as the abducting eye
- DIPLOPIA
- HORIZONTAL NYSTAGMUS of the abducting eye
(pupillary light reflex and convergence are preserved)
Jugular Foramen Syndrome
cause? s/s?
think about what goes thru the jugular foramen
tumor, trauma or infection affection affecting structures that pass thru the jugular foramen (CN IX, X, XI, jugular vein)
- posterior 1/3 taste loss (CN IX)
- gag reflex loss (CN IX, X)
- dysphagia (CN IX)
- dysphonia/hoarseness (CN X)
- soft palate drop; uvula toward unaffected side (CN X)
- SCM and trapezius paralysis = “shoulder drop” (CN XI)
Main SC tracts affected in subacute combined degeneration (3)
- DORSAL COLUMN - position/vibration (proprioception); sensory ataxia with POSITIVE ROMBERG
- SPINOCEREBELLAR TRACT - ataxia
- LATERAL CORTICOSPINAL - spastic paresis
Romberg test
Premise = patient needs at least 2 of the 3 systems of proprioception, vestibular system and vision to maintain balance
Normal pt can close eyes and still have proprioception and vestibular system to maintain balance
POSITIVE ROMBERG pt closes eyes and cannot balance because both vision and PROPRIOCEPTION IMPAIRED (as in dorsal column damage, like subacute combined degeneration in B12 defic.)
MAIN SC LESIONS in poliomyelitis / spinal muscular atrophy (aka Werdnig-Hoffman)
loss of anterior horn motor neurons
causes FLACCID PARALYSIS, atrophy and fasciculations (twitches)
MAIN SC LESIONS in multiple sclerosis
pattern is RANDOM and ASYMMETRIC
MAIN SC LESIONS in tabes dorsalis of tertiary syphilis
ONLY the DORSAL COLUMNS and DRGs
as opposed to SCD which affects lateral corticospinal and spinocerebellar tracts as well
MAIN SC LESIONS in syringomyelia
central cavitation affects the ANTERIOR WHITE COMMISSURE of the SPINOTHALAMIC TRACT
(is usually cervical > BILATERAL PAIN/TEMP LOSS in UPPER LIMBS, may progress to legs
can expand to ventral horns > flaccid paralysis of hands)
Syringomyelia
most common location of dilation
C8 to T1 levels of SC
extends rostral, caudal and centrifugal
Syringomyelia
what skeletal sx is seen and why?
kyphoscoliosis
paresis of paravertebral muscles
Neuroblastoma
cell origin + where is it? who gets it?
what are the main signs (4) clinically?
neural crest cells
in adrenal medulla + sympathetic chain of kids <2
- Abdominal Mass
- Periorbital bruise (metastases)
- Opsoclonus-Myoclonus - eye, trunk + limb jerking
- “DUMBBELL TUMOR” appearance on imaging due to sc compression/epidural invasion
What is the general progression of muscle weaknesses associated with lumbosacral radiculopathy from L2 to S1?
- Generally higher segments (L2 - L4) will affect HIP FLEXION and KNEE EXTENSION (picture a crane kick)
- Lower segments (L5 - S1) will affect FOOT movements, HIP EXTENSION and KNEE FLEXION (picture a superman stretch)
What two lumbosacral radiculopathy segments affect important reflexes and which reflexes?
L4 - affects the PATELLAR REFLEX
S1 - affects the ACHILLES REFLEX (“ankle jerk reflex”)
Subacute Cerebellar Degeneration
cause? s/s? labs?
paraneoplastic issue from SCLC, breast, ovary and uterine tumors
progressive dizziness, limb/trunk ataxia, dysarthria, visual disturbance (diplopia, oscillopsia)
anti-tumor Abs cross react with Purkinje cell Ags > acute-onset rapid cerebellar degeneration
antibodies are anti-Yo, anti-P/Q and anti-Hu
Bilateral anterior cerebral artery occlusion can cause what?
Sensorimotor - leg/foot numbness + weakness
BEHAVIORAL SX - abulia (lack of will/initiative - prefrontal)
INCONTINENCE - frontal micturition center; medial frontal lobe + cingulate gyrus
Mnemonic for which CNs are sensory, motor and both
Some Say Marry Money But My Brother Says Big Brains Matter Most
Vagal Nuclei
3 and what they do
- nucleus Solitarius - visceral Sensory info (VII, IX, X)
- nucleus aMbiguus - Motor innervation of pharynx, larynx and upper esophagus (IX, X, XI)
- dorsal motor nucleus - autonomic fibers to heart, lungs and GI (X only)
ALS
lesions + s/s
UMN and LMN lesions (corticobulbar/-spinal and medullary/SC anterior horn)
LMN - dysarthria, dysphagia, asymmetric limb weakness, fasciculations, atrophy
UMN - pseudobulbar palsy (facial movement disorder also with dysarthria/-phagia), emotional lability, spastic gait, clonus
ALS
enzyme deficit + treatment
SUPEROXIDE DISMUTASE 1
tx is with RILUZOLE, but is still fatal
Cerebral Amyloid Angiopathy
is the MCC of what? and what areas of the brain does it affect?
CAA is the mcc of SPONTANEOUS LOBAR HEMORRHAGE, especially in pts > 60
tends to be RECURRENT and in OCCIPITAL / PARIETAL LOBES (frontal rarer, but possible)
Considering what parts of the brain it mostly affects…
what are the clinical results of CEREBRAL-AMYLOID ANGIOPATHY-related lobar hemorrhage?
occipital - HOMONYMOUS HEMIANOPSIA
parietal - CONTRALATERAL HEMISENSORY LOSS
(frontal - more rare, but CONTRALATERAL HEMIPARESIS)
Hypertensive encephalopathy
presentation?
PROGRESSIVE headache > nausea + vomiting
NONLOCALIZED neuro sx (confusion, etc.) in setting of hypertension
differential between cerebral hemorrhage due to AVM and cerebral amyloid angiopathy
AVM - a SINGLE lesion in a CHILD
CAA - MULTIPLE lesions in an OLDER ADULT (esp. parietal / occipital)
What is “pseudotumor cerebri”?
other name? in whom? presentation?
“Idiopathic Intracranial Hypertension”
YOUNG OBESE WOMEN
- daily HEADACHE
- bilateral symmetric PAPILLEDEMA (optic disc edema with blurred borders on funduscopy)
- TRANSIENT visual disturbances - worsened by Valsalva (bend down, cough, etc.)
Broca aphasia
spontaneous speech? comprehension? repetition?
sparse + nonfluent speech (slow and mostly nouns + verbs)
PRESERVED comprehension
impaired repetition
Broca aphasia
area damaged? associated features?
INFERIOR FRONTAL gyrus of the dominant (usually LEFT) hemisphere (Br. 44 + 45)
associated FACE + ARM HEMIPARESIS (usually right-sided, due to proximity of lesion to primary motor cortex)
Wernicke aphasia
spontaneous speech? comprehension? repitition?
Fluent + voluminous NONSENSICAL speech
DIMINISHED comprehension
impaired repetition
(also lack insight)
Wernicke aphasia
area damaged? assoc. features?
POSTERIOR SUPERIOR TEMPORAL gyrus (Br. 22) usually of the dominant (left) hemisphere
assoc. with SUPERIOR VISUAL FIELD DEFECT (usually R sided)
Frontal eye field
where is it? what does a lesion here cause?
POSTERIOR MIDDLE FRONTAL gyrus (just above Broca area)
lesion causes EYE DEVIATION to IPSILATERAL SIDE
What is CONDUCTION APHASIA?
spontaneous speech? comprehension? repetition?
fluent with PHONEMIC errors (as in saying “thumb” instead of “dumb”… replacing one phoneme with another)
PRESERVED comprehension
VERY POOR repetition
what is damaged in CONDUCTION APHASIA?
the ARCUATE FASCICLE
connection btwn Broca and Wernicke areas within frontal + parietal lobes
Meningioma
common sites + resulting sx
dural reflections
eg, falx cerebri, tentorium cerebelli
falx > disruption of contralateral LEG sensation/motor (due to location on homunculus)
What is the major difference in seizure type that determines whether broad spectrum or narrow spectrum anti-epileptics should be used?
Focal vs. generalized
focal = 1 hemisphere AT ONSET = narrow spectrum
generalized = both hemispheres AT ONSET = broad spectrum
what is the difference between “simple” and “complex” seizures?
simple = no lost consciousness
complex = lost consciousness
Huntington disease
inheritance? gene affected?
AD inheritance - history in 1st deg relative
increased CAG repeats in HTT gene on Chr. 4 for Huntingtin protein
(in Huntington the Caudate has less Acetylcholine and Gaba … CAG; “hunt” is 4 letters > chr. 4)
Huntington disease
sx onset? s/s?
onset at 20-50 yrs old (dep on anticipation); 35-45 most common and will live 15-20 yrs after
CHOREA - from fidgeting to uncontrollable swinging of limbs
DEMENTIA - memory + cognitive decline
BEHAVIOR - aggressive, apathy, depression
Huntington disease
macro + micro brain changes
Macro - CAUDATE ATROPHY with some putamen/frontal atrophy
Micro - NEURON LOSS in CAUDATE/PUTAMEN
Huntington disease
decreased what where?
mechanism of neuron damage?
decreased ACh, GABA and Substance P in “striatum” (caudate + putamen)
excitotoxicity - NMDA-Rs bind Glu and overexcite > neuronal death
injury to WHAT nerve WHERE can cause Trendelenburg gait?
injury to SUPERIOR GLUTEAL NERVE in the SUPEROMEDIAL quadrant of a buttock
will paralyze the ipsilateral gluteus medius/minimus and cause contralateral Trendelenburg
ie, left nerve issue will weaken left abductors > right hip will drop when right foot is lifted during walking
(common in IM injection in wrong place, give superolateral or anterolateral buttock)
Hypothalamic Nuclei: what is the function of…
ventromedial?
satiety
damage > hyperphagia
(remember medial + lateral oppose each other’s actions in appetite regulation
“I SAT MEDitating then HUNG LANTerns”)
Hypothalamic Nuclei: what is the function of…
lateral?
hunger
damage > anorexia
(remember medial + lateral oppose each other’s actions in appetite regulation
“I SAT MEDitating then HUNG LANTerns”)
Hypothalamic Nuclei: what is the function of…
anterior?
heat dissipation
damage > hyperthermia
(remember ant + post oppose each other’s actions in temp regulation
“I DISliked my AUNT’s CONSERVative POST on Facebook”)
Hypothalamic Nuclei: what is the function of…
posterior
heat conservation
damage > hypothermia
(remember ant + post oppose each other’s actions in temp regulation
“I DISliked my AUNT’s CONSERVative POST on Facebook”)
Hypothalamic Nuclei: what is the function of…
arcuate?
secretion of DOPAMINE > prolactin inhibition
GHrH and GnRH release also
Hypothalamic Nuclei: what is the function of…
Paraventricular?
ParaVenTriCular
Vasopressin (and oxytocin)
Thyrotropin-releasing hormone
Corticotropin releasing hormone
(look for the V T C in VenTriCular + oxytocin/vasopressin go together)
Hypothalamic Nuclei: what is the function of…
Supraoptic?
SuprAOptic
ADH
Oxytocin
Hypothalamic Nuclei: what is the function of…
Suprachiasmatic?
SupraChiasmatic
Circadian rhythm + pineal function
Cognitive testing for…
COMPREHENSION
follow a MULTISTEP COMMAND
Cognitive testing for…
CONCENTRATION / ATTENTION
Recite months BACKWARDS
Count DOWN from 100 by 7s
Spell “world” BACKWARDS
Cognitive testing for…
SHORT TERM MEMORY
Repeat 3 unrelated words AFTER 5 MINUTES
Cognitive testing for…
LONG TERM MEMORY
Recall PAST LIFE EVENTS
Cognitive testing for…
VISUAL-SPATIAL
DRAW INTERSECTING PENTAGONS
Cognitive testing for…
EXECUTIVE FUNCTION
DRAW a CLOCK oriented to a REQUESTED TIME
Dementia dx criteria (2)
- Impairment in AT LEAST ONE cognitive domain
2. FUNCTIONAL IMPAIRMENT in daily life
Spinal Stenosis
3 pathophysiological changes in spine
- LIGAMENTUM FLAVUM thickening - compresses SC
- Hypertrophic FACETS - on vertebrae, plus…
- DISC BULGING - both cause foraminal stenosis
Spinal Stenosis
sx (3)?
what exacerbates / improves the pain?
- leg pain
- numbness / paresthesia
- weakness
WALKING worsens pain (“neurogenic claudication”) as well as anything that EXTENDS LUMBAR SPINE (due to further canal narrowing)
LUMBAR FLEXION decreases pain (leaning on shopping cart, walking uphill)
Spinal Stenosis
MCC
Osteoarthritis of the spin
mostly pts > 60
What is the cause of…
UNILATERAL vs. BILATERAL internuclear ophthalmoplegia?
unilateral - stroke, usually older pt
bilateral - MS, usually younger pt
What are the 2 neuron types / areas in the CNS most vulnerable to hypoxic injury via ischemia?
- PURKINJE cells of cerebellum
2. PYRAMIDAL cells of hippocampus and neocortex (zones 3, 5, 6)
What GENERAL areas of the brain are susceptible to ischemia?
watershed regions between areas supplied by ACA, MCA and PCA
What/where is the FRONTAL EYE FIELD?
Activation of a UNILATERAL frontal eye field (as in seizure) causes what?
cerebral cortical region that controls HORIZONTAL EYE MOVEMENT; located just above Broca’s area
activation of one side causes EYE DEVIATION TO OPPOSITE SIDE
(but after a seizure “post-ictal neuroinhibition” of that area would cause deviation to the same side)
