neuro Flashcards
what kind of pathology would result in such a lesion
destruction of LMNs
i.e. polio, Werding-Hoffman Ds (group of inherited diseases that are characterized by progressive weakness of the muscles and reduced muscle tone)
present as flaccid paralysis, muscle atrophy, and fasciculations
what kind of pathology would result in such a lesion
MS= a demyelinating disorder affecting the white matter of the CNS in random and assymetric pattern
= dif neuro deficits across space and time
what kind of pathology would result in such a lesion
degeneration of dorsal root columns
the only (SC)manifestion of this is loss of touch, vibration, and proprioception
-tabes dorsalis= tertiary syhphillis = degneration of the dorsal root ganglia and DCML
what kind of pathology would result in such a lesion
x dorsal columns (touch, vibration, proprioception)
x lateral corticospinal tract (spastic paresis)
this occurs in Vit B12 (cobalamin) deficiency= subacute combined degeneration
=x dorsal columns, lateral corticospinal tract, +spinocerebellar (ataxia)
=will also have atrophic glossitis (big, glossy tongue)
—> ds results from pernicious anemia (autoimmune gastritis w low IF), gastrectomy, ileal resection, diphyllobothrium latum infection (tapeworm)
what kind of pathology would result in such a lesion
this is an injury to the anterior white commissure of the spinal thalamic tract
=syringomyelia (cape distribution, central cavitation of the cervical cord) –>bilat loss of pain and temp of the UE
-if it expands into the ventral horn –> flaccid paralysis of the hands
in the setting of pancoast tumors, what diff structures could be compressed and cause sx
- brachial plexus : ipsi shoulder pain, UE parasthesias, areflexic arm wknss
- cervical sympathetic ganglia = horner’s syndrome
=ipsi ptosis, miosis, anhidrosis
brain tumor
what is this, how does it present
biopsy shows a meningioma
red arrow: whorled grown of (meningeal) cells that are forming syncitial nests
black arrows: nests have calcified into lamellar structures aka psammoma bodies
round masses attached to the dura, commonly found at falcine= present with seizures, w compression of the adjacent structures.
-slow growing: HA, N/V –> inc ICP, (worse w recumbency and sleep) in intracranial volume
brain tumor
what is this, how does it present
adamantinomatous craniopharyngitis = benign suprasellar tumors in children
cords/nests of pallisading squamous epithelium with internal areas of lamellar “wet” keratin under light microscopy
what brain tumor is this
ependymoma = paraventricular tumors (i.e. floor of the 4th ventricle)
of the ependymal cells that line ventricles
this is the most common primary malignant brain tumor in adult
describe its anatomy and histo findings
glioblastomas
often in the cerebral hemisphere and may cross the corpus callosum (butterfly glioma)
histo = hypercellular areas of atypical astrocytes border areas of necrosis
malignagnt brain tumor in children composed of small blue cells
what is the other classical histologic finding
medulloblastoma
the small blue cells surround neuropil = homer-wright rosettes under lightmicroscopy
what brain tumor is this
showing what classical finding below (round nuclei surrounded by halo of clear cytoplasm)
oligodendroglioma
in the white matter of cerebral hemispheres, tumors with fried egg appearance
what benign brain tumor is this?
showing eosinophilic granular bodies around elongated fibers on histo
clinical presentation
pilocytic astrocytoma
the elongated, hair like processes = rosenthal fibers
in cerebellum of children and YAs
what brain tumor commonly arises from CN VIII at the cerebellopontine angle?
what are the histo findings?
schwannoma = mostly benign
arise from vestibular branch of CN VIII at the cerebellopontine angle
histo= spindle cells with pallisading nuclei arranged around Verocay bodies (eosinophilic cores ) = Antoni A pattern
what three organisms cause meningitis in neonates (0-3 months)? what 2 organisms cause meningitis in older infants (>3 months)?
what lab/microscopy findings set them apart from each other
grp b strep
- G+ cocci, facultative anaerobe
- capable of complete hemolysis, catalase -
e. coli:
- G -, motile, facultative anaerobe, rod,
- ferments lactose and glucose
- can grow on blood, MacConkey (bc of the lactose), eosin Methylene blue agar plates
listeria monocytogenes
- G+ rod, motile, grows in cold
- NONspore forming, use lysteriolysin O to skip phagolysosomes
strep pneumo
- G+ cocci, facultative anaerobe
- alpha hemolytic, catalase -, capsulated
n. meningitidis - G- dipplococci, facultated anaerobe
- capsulated, endotoxin LPS
which virus is the most common cause of fatal sporadic encephalitis
etiology?
HSV-1
what is the etiology that predisposes people to migraines/aura? what does aura look like?
–inc cerebral excitability –>a wave of corticol spreading depression
-aura can be visual or sensory (i.e. unilat extremity parasthesias)
=abn activation of trigeminal afferents–> spreads to the meninges and intracranial vasculature –> release calcitonin-gene related peptide (CGRP) ∝ pain transmission
-CGRP also causes local vasodilation and inc neurogenic inflammation –> worsens pain
what 3 systems send signals to the medullary vomiting center to cause N/V
what NT and receptors are used
GI = irritation (infection, chemo, distension)
=send 5-ht3 (serotonin) from the stomach –> vagal + spinal afferent Ns –> medullary VC,
and CN XI from the tongue directly
vestibular system= motion sickness and vertigo
H1+ M1 receptors in ear send signal to medulla via CN VIII
chemoreceptor trigger zone =
emotogenic substances activate D2 receptors in the area postrema, right next to the vomiting center
what are the specific indications for the following bipolar drugs, and what are the AE of each
lithium
valproate
carbamezapine
lamotrigine
where are wernicke’s area and broca’s area + Brodmann’s area #s
(be able to point it out or use your words)
wernicke = posterior section of the superior temporal gyrus, L = brodmann’s area 22
broca = pars opercularis and pars triangularis of inferior frontal gyrus, L = brodmann’s 44+45
where are the
primary visual cortex,
the primary auditory cortex,
primary motor cortex
primary somatosensory cortx
primary visual cortex = posterior occipital lobe
the primary auditory cortex= superior temporal lobe
primary motor cortex = precentral gyrus
primary somatosensory cortx = postcentral gyrus
where are the each of the following located, and what is their function
- somatosensory association cortex
- premotor cortex
- frontal eye field
- prefrontal cortex
- limbic association area
- arcuate fasciculus
- somatosensory association cortex
- directly posterior to post-central gyrus, parietal lobe
- higher mental and emotional processes, including memory, learning, speech, and the interpretation of sensations
- premotor cortex
- anterior to primary motor cortex, frontal lobe
- associated w Ms of the trunk
- frontal eye field
- intersection of the middle frontal gyrus and the prefrontal gyrus
- saccadic eye movements for visual field perception and awareness, and voluntary eye movements
- communicate w extraocular Ms via paramedian pontine reticular formation
- lesion = deviation of eyes to ipsilateral side
- prefrontal cortex
- front part of frontal lobe
- planning complex cognitive behavior, personality expression, decision making, moderating social behavior
- limbic association area
- medial side of frontal lobe
- helps form memories and translate that to motor responses
- also help processes emotion and guides emotional response
- arcuate fasciculus
- a fiber tract connecting caudal temporal cortex and inferior frontal lobe
- bundle of axons that connects broca’s and wernickes areas
- a fiber tract connecting caudal temporal cortex and inferior frontal lobe
what is the difference between schizoid personality and avoidant personality
schizoid: content w being alone from people, voluntary withdrawal from others, limited emotional expression
avoidant: hypersensitive to rejection and criticism, socially inhibited and timid, but desires relationships with others
what kind of neurotransmitter is glycine (activating/inhibiting)
what is glycine encephalopathy
inhibiting
glycine encephalopathy = congenital defect in glycine metabolism
–> myclonic seizures and rapidly progressive, eventually ends in respiratory distress
–> floppy baby syndrome
myasthenia gravis is due to antibodies to what receptor type specifically
nicotinic Ach R
what is the difference between partial (2) and generalized (5) seizures?
list and describe the types of each
partial seizures = focal, single area of brain effected (mc in medial temporal lobe)
- simple partial: pt retains awareness/consciousness : can be motor, sensory, autonomic, psychic
- complex partial: impaired consciousness, movements made without conscious thought or intentions (automatism)
general seizures = diffuse brain damage
- petit mal= absence seizures= blank stare, no postictal confusion, 3 hz spike and wave discharges
- myoclonic= quick, repetitive jerks
- grand mal = tonic-clonic= alternating stiffening and movement, postictal confusion, urinary incontienence, tongue biting
- tonic = stiffening
- atonic= drop seizures (falls to floor), commonly mistaken for fainting
an eye that is down and out, dilated, and ptosis –suggests what pathology
oculomotor nerve palsy associated w posterior communicating A
what antipyschotics can be used for schizophrenia
olanzapine, clozapine
aripiprazole, asenapine, quetiapine,
iloperidone, paliperidone, risperidone
lurasidone, ziprasidone
what structures are derived from neural crest cells
PNS and surrounding structures
*MOTEL PASSES*
Melanocyte
Odontoblasts
Tracheal cartilage
Enterochromaffin cells
Leptomeninges (arachnoid, pia)
PNS ganglia (cranial, dorsal root, autonomic)
Adrenal medulla
Schwann cells
Spiral membrane (aorticopulmonary septum)
Endocardial cusions (+ mesoderm)
Skull bones
what is the clinical presentation of toxoplasmosis
how is it transmitted
how is it treated
immunocompromised patient comes in w seizures, brain CT/MRI shows ring enhancing lesions in the frontal and parietal lobe = brain abscesses
+chorioretinitis, lymphadenopathy, fever, focal weakness,
transmission of toxoplasma gondii:
inhale from cat feces, consume cysts in undercooked meat
trx=
acute: sulfadiazine + pyrimethamine
prophylactic: antiretroviral therapy; TMP/SMX for those w CD4<200
what is the trx of an acute cluster HA
100% oxygen + sumatriptan/zolmitriptan
**triptans = 5HT1 receptor agonists, also used in acute migraines
what trx is given to prevent the development of seizures in the setting of pre-eclampsia with severe featurs
- give magnesium = to prevent seizures
- induce labor w oxytocin
what is somatic sx disorder
= 1 or more somatic sx that are distressing or result in significant disruption of daily life
- disproportionate and persistant thoughts about the seriousness of the sx
- high levels of anxiety about one’s health or sx
- spending excessive time/energy on one’s health or sx
*
what structure in the brain makes up the “vomiting center”
where does it receive input from
NTS= nucleus tracus solitarius
- in medulla: coordinates responses from other medullary centers
- input from GI tract (serotonin activated CN X), vestibular system (CN VIII-motion sickness), area postrema (in the 4th ventricle, responds to changes in blood and CSF, especially chemo agents)
people with panic disorder are at increased risk of developing what phobia
agorophobia
fear of going out and being in situations they can’t get out of = avoid situations where they might be trapped or helpless in the event of another panic attack
Down syndrome is related to what complications in each of the following systems
- neuro
- cardio
- GI
- endo
- heme
- rheumatology
- neuro
- early onset Alz (AB amyloid, early on show high levels of amyloid precursor protein
- cardio
- septal defects
- GI
- duodenal atreisa and hirschprung
- endo
- hypothyroid, type 1 diabetes, obesity
- heme
- acute leukemia
- rheumatology
- atlantoaxial instability
opiates act on which receptors on which side of the synapse, causing what change in which ion movement
where are the receptors found
mu receptors, in the spine
- work PREsynpatically to reduce Ca influx –> dec excitatory NT release
- work POSTsynpatically to open K channels –> K efflux –> membrane hyperpolarization
speed of conductance down an axon is based on what two things?
the length constant : how far down an axon an electrical impulse can propogate without requiring regeneration
-depends on the resistance to conductance
the time constant : how long it takes the membrane potential to respond to a change in membrane permeability
-depends on membrane resistance and capacitance
thiamine deficiency will affect what 4 enzymes in what 4 pathways
niacin deficiency will affect what
x thiamine
- pyruvate dehydrogenase
- pyruvate –> acetyl CoA (citric acid cycle)
- alpha ketoglutarate dehydrogenase (citric acid cycle)
- branched chain alpha keto-acid dehydrogenase (AA catabolism)
- transketolase = for PPP
x niacin =
- x NADPH + NADP
- x glutathione reductase :metabolism of harmful reactive oxygen species (ROS)
- common presentation of MG
- pathophys of the ds
- trx
-MG = weakness worse at night, better in morning
- often can present with diplopa/ptosis, difficulty chewing, etc
- auto-Ab against post-synaptic nAchR –> endocytosis of the receptors –> reduced amplitude of end motor plate action potential in response to stimulation –> dec M firing
- trx w anticholinesterase, immunosuppression, and a thymectomy
- the anticholinesterase such as pyridostigmine, which is not N/M specific, would cause mAchR ovestimulation– so use N specific drugs= glycopyrrolate, hyoscyamine, propantheline
where in the synapse is the mechanism of action of the botulinsm toxin?
organophosphates?
botulin toxin = blocks pre-synpatic Ach release into both nAchR and mAchR
organophosphates = AchE-inhibitors
which brain tumor presents with a biphasic histologic pattern with highly cellular cells mixed w myxoid regions of low cellularity
-what other histologic finding is associated with these tumors
how do these tumors present, where are they usually found
Schwannomas
highly cellular cells = Antoni A pattern
myxoid regions of low cellularity = Antoni B pattern
- also see Verocay bodies = palisading patterns w interspersed nucear free zones
- MC at cerebellopontine angle
- usually present w tinnitus, vertigo, and hearing loss
S-100 is a marker for what tumor origin
-which are S100 (+)
neural crest origin
=melanoma and schwannomas
what physical exam findings are shown below?
- what is the embryologic origin of these lesinos
what is the dx, inheritance, and what other exam findings do you expect to see
NF1 = AD ch 17
- cutaenous neurofibromas = hallmark
- numerous, fleshy, dome shaped/pedunculated lesions that vary size: usually multiple, disperse across the body
- = made from schwan cells –> from neural crest cells
- cafe au lait spots
- patches of hyperpigmented skin (light brown spots) that are either smooth or irreguar borders
- may be associated with axial or inguinal freckles
- optic N glioma
- can cause vision loss
- Lishc nodules
- pigmented, asymptomatic hamartomas of the iris
- bone abnormalities
- congenitial psuedoarthritis, scoliiosis, sphenoid dysplasia
- other tumors
- meningiomas, astrocytomas, gliomas, pheochromocytomas
pt presents w hx of sudden, explosive headache –> loss of conscioussness –> regain consciousness, now with signs of meningeal irritation
dx?
how will their mental status fair moving forward? any complications?
SAH
- will probs have been alert when they woke up, but now will have deterioting consciousness and have somnolence
- a few days later, vasospasm may cause sudden worsening of sx again
-present w blood layering the sulci
MRI diff between epidural, subdural, and SAH
fracture of the cervical spine transverse foramine can injure what big A?
this A lets off what branch that results in a characteristic spinal cord syndrome? describe teh syndrome
vertebral A runs through the transverse foramina of the C spine
PICA will branch off of it up near the lateral medulla –> lateral medullary syndrome aka Wallenberg syndrome
functions of the CN VII
lesion causes what syndrome, presents how?
CNVIi = facial N
function:
- motor output to facial Ms
- para innervation to lacrimal ,submandibular, sublingual salivary glands
- taste ant 2/3 tongue
- somatic afferent pinna and external auditory canal
x= bell’s palsy
- suddent onset unilat facial M wkns
- =trouble opening eye, uneven smile, thinnning of nasolabial fold
- ipsi eyebrow sag and mouth droop
- may have dec tearing and taste on that side
**preserve palate movement = CN 9+10**
where is the locus ceruleus
- function?
- effects of loss?
locus cerulus = pigmented nucleus at the posterior rostral pons at the lateral floor of the 4th ventricles
= principle site of NE synthesis
associated w mood, arousal (reticular activating system-RAS), sleep-wake cycles, cognition, autonomics
- dysfunction associated w anxiety disorders
- lose one side = impaired consciousness, extensor posturing, pinpoint pupils
- bilat pontine hemorrahage= coma bc no activation of RAS
a pt recently started on antipsychotics who now complains of suddent onset M stiffness or spasms is experiencing what?
- likely cause?
- pathophys?
- trx?
acute dystonic reaction aka spasmodic torticollis
=a type of EPS sx in response to the antipsychotic
- most likel causes= haloperidol and fluphenazine
- pathophys = Dopamine - Ach imbalance
- the niagrostiatal pathway requires both Dopamine (D2) and Ach (M1) to balance each other out
- D2 antagonists (antipsychotics) will remove the inhibitory effect of dopamine –> constant activation of M1 receptors –> inc movement, spasticity –> pain and stiffness
- can be in major muscle groups, in just eye movements, in the laryngeal Ms. …
- trx with M1 receptor antagonists co-administration to re-establish balance
- i.e. benztropine
- can also trx w an antihistamine = diphenydramine
lesion of the anterior cerebral A–> ?
unilat vs bilat
x supply to the medial ipsi hemisphere = x sensory motor to contra foot and leg
- i..e climbin stairs
bilat= behavioral changes (i.e. inablity to lie, x willpower) and urinary incontinence
compare the blood solubility and the blood:gas coefficient of drug A with nitrous oxide
what does they say about their action as inhaled anesthetics
drug A has a higher blood solubility which is why it takes longer for it to reach the plateau PARTIAL PRESSURE than it it took NO
higher blood gas solubity = higher blood gas coefficient = slower ONSET OF ACTION
(nothing to do w potency aka how much you need)
what is the shared etiology of spina bifida oculta, meningocele, and meningomyelocele and how are they different
how can they be detected in utero
what are risk factors
how are they all different from anencephaly (which will present how)
all= failure to caudal neuropores to fuse in wk 4
- they all have the defect in bony formation of the vertebra
- detect w US, inc AFP (+inc AchE for confirmation)
- risk= maternal diabetes, dec folic acid (happens before mom knows shes preg), maternal obesity, maternal use of valproic acid or carbamezapine
spina bifida oculta= bony malformation but dura is intact and nothing comes out
- have tuft of hair or skin dimple at level of bony defect
meningocele
- meninges alone protrudes out of the hole in the bone, associated with spina bifida cystica
meningomyelocele
- meninges and neural tissue (i.e. cauda equina) herniate through the bony defect
- almost always associated with a chiari malformation, which will inc the P and push he out
vs ANENCEPHALY = failure of rostral neuropore to close –> open calvarium which leaves the forebrain and brainstem exposed in utero so they don’t develop normally
- not compatible with life- will die in utero or shortly thereafter
- “frog-like” appearance of the fetus
- associated with polyhydramnios bc the there is no swallowing center in the fetal brain to drain out the fluid made
brainstem anatomy
- general location of the CNs
- blood supply to the regions
MIDBRAIN
- CNs
- medial = 3+4
- BS
- medial <–PCA –> lat
PONS
- CNs=
- medial = 6 —— lateral = 5,7,8
- BS=
- medial = basilar A : lateral = AICA
MEDULLA
- CNs=
- medial = 12 — lateral = 9, 10, 11
- BS=
- medial= ASA — lateral = PICA
contents of the cavernous sinus
what sinus is it located directly above, and what structure is it directly below
internal carotid A
CN 3, 4, 6, V1+V2
right under pituitary gland, right above sphenoid sinus
what is this physical exam finding
- what is the etiology
what non-neoplastic pathology is often associated with this
- classic presentation
papilledema = blurred and enlarged optic disk
- inc P –> compress optic N –> dec axoplasmic flow –> bilateral optic disk edema
associated with pseudotumor cerebri
- =intracranial HTN that presents in young women who have daily HA and transiet visual changes
- worse with valsalva bc it inc the P
- a white pupillary reflex is associated with what pathology?
- this pathology is associated with a mutation in what gene?
- germline mutation of this gene is associated with inc risk of what?
- retinoblastoma ∝ white pupillary reflex
- ∝ with xRb (~40% are familial, rest are not ) –> associated w 2 hit hypothesis (inc risk w germline mutaiton bc any one chr only needs one hit)
- inherited x Rb is associated w increased risk of osteosarcoma and other sarcomas
what structures are derived from neural crest vs neural tube vs surfact ectoderm
neural TUBE = CNS tube
neural crest =
- ganglia + schwann cells + adrenal medulla
- heart septum and endocardial cushions
- branchial arches (–> bones and cartilage) + skull bones
- melanocytes
MOA of
- inhaled anesthetics
- IV anesthetics
- local anesthetics
- inhaled anesthetics
- unknown
- ”“-urane”s and N.O
- IV anesthetics
- facilitate GABA (ketamine via NMDA antagonism)
- local anesthetics
what drugs are used to treat Parkinsons, and what is their MOA
bromocriptin + pramipexole = dopamine agonists
what exits through the
- superior orbital fissure
- foramen ovale
- foramen rotundum
- foraem spinosum
- jugular foramen
a child presenting with extremity weakness and abn involuntary (choreoathetoid) movements, cognitive and motor delay, and growth development delay and levels of arginine suggests what pathology
arginase deficiency
= no make urea –> build up of arginine –> toxic
-no hyperammonia seen*
age related visual loss is often associated with what
sx and clinical presentation
cataracts = gradual opacification of the eye
sx= gradual vision loss, excessive glare from bright lights,
clin= loss of red reflex
the middle meningeal A branches off of what A
the MAXILLARY A
what are the adrenergic receptors on the
- eye
- bladder
- uterus
and what are their effects
describe the 3 Ns that carry sensation to the tongue
preventative vs abortive migraine medication
inhaled anaesthetics can cause what undesired effects in what 5 organs
which cranial Ns are the afferent and efferent in each of the following reflexes
- pupillary light reflex
- corneal reflex
- jaw jerk reflex
- vestibuloocular reflex
- carotid sinus reflex
- cough reflex
- gag reflex
where are each of these and what structures can be compressed the following herniations
- subfalcine herniation
- transtentorial herniation
- tonsillar herniation
- subfalcine herniation
- cingulate gyrus herniates under the falx cerebri
- potentially compress ACA
- transtentorial herniation
- when the medial temporal lobe (uncus) herniates between the crus cerebri and tentorium cerebelli
- can compress ipsi CNIII, ipsi PCA, contra cerebral peduncle (–>ipsi hemiparesis), stretch/rupture of the basilar A (–>hemorrhage into midbrain/pons –> fatal)
- tonsillar herniation
- cerebellar tonsils through foramen magnum
- compress medulla
what is the pathway in the brain that leads to parkinsonian symptoms
what AEs can emerge with long term treatment of PD w levodopa
high frequency stimulation of what part of the brain can treat PD motor sx?
- degeneration of the striatum and substanita nigra –> excessive excitation of the globus pallidus internus from the subthalamic nucleus (now unchecked) –> excessive inhibition of the thalamus
levodopa >5 years –> motor fluctuations and dyskinesia
- motor fluctuations : good mobility when the drug is at higher concentrations in the body, but then increased bradykinesia and rigidity when the concentrations falls/drug wears off
- dyskinesia: excessive involuntary movements during periods of increased drug concentrations
high frequency deep brain stimulation of the globus pallidus or subthalamic nucleus –>thalam-cortical disinhibition –>better mobility
what is anterior cord syndrome
the lesion and the sx
Alzheimers is associated with atrophy of the temporoparietal hemispheres and the hippocampus (hippocampal is present early in the ds)
