Neuro Flashcards

Question

What are the symptoms of osmotic demyelination syndrome? Pathophys? What usually causes it? What related syndrome causes cerebral edema?

Answer 1

Acute paralysis, dysarthria, dysphagia, diplopia, and loss of consciousness Massive axonal demyeination in white pontine matter secondary to osmotic changes Correcting hyponatremia too fast (add sodium, water rushes out of axons) From low to high, your pons will die (osm. demy syn) From high to low, your brain will blow (edema/herniat)

Answer 2

Modulates movement; aids in coordination and balance Input: Contralateral cortex via middle cerebellar peduncle Ipsilateral proprioceptive info via inf. cereb. ped. from spinal cord Output: To contralateral cortex to modulate movement via purkinje nerves (purkinje to deep nuclei to contralateral cortex via cerebellar peduncle Deep: Dentate, emboliform, globose, fastigial (Don't Eat Greasy Foods) Lateral: voluntary movment of extremities; when injured propensity to fall toward injured side Medial lesins: Midline structures and/or flocclonodular lobe=truncal ataxia (wide based cerebellar gait), nystagmus, head tilting. Bilateral lesions affecting axial and proximal limb muscles

Answer 3

Voluntary movements and making structural adjustments Receives cortical input (negative feedback to cortex to modulate movement) substantia nigra pars compacta globus pallidus (internus and externus) subthalamic nucleus striatum (putamen + caudate) INdirect=INhibitory (less direct pathway-more steps) Direct=facilitaes movement Direct: Striatum inhibits the GPi from inhibiting the thalamus. Then, the thalamus facilitates movement Indirect: Striatum inhibits the GPe from inhibiting the STN. The STN then stimulates the GPi so it greatly inhibits the thalamus from stimulating movement. The pars compacta releases dopamine. The direct pathway has a D1 receptor and the independent pathway has a D2 receptor. D1 receptor is stimulatory and D2 is inhibitory. Therefore, dopamine stimulates movement through both pathways. D1Receptor=D1Rect substantia pars reticula functions much like the GPi.

Answer 4

Ath: slow writhing movements, especially in fingers (BG/Caudate/Hunting) Chorea: Sudden jerky purposeless movements (BG/Caudate/Hunting) Dystonia: sustained involuntary muscle contractions (writers cramp and sustained eyelid twitch) Hemiballismus: sudden, wild flailing of 1 arm and may ipsilateral leg (Contralateral Subthalamic nucleus) Myoclonus: sudden, brief, uncontrolled muscle contraction (jerks, hiccups=metabolic abnormalities such as renal and liver failure)

Answer 5

High frequency tremor with sustained posture (outstretched arms) Worse with movement or when anxious Familial Self medicate with EtOH (decr. amplitude of tremor) Beta blockers and primidone Slow, zigzag motion when pointing/extending toward a target Cerebellar dysfunction Uncontrolled movement of distal appendages at rest Alleviated by intentional movement parkinsons Pill rolling tremor.

Answer 6

``` Degenerative disorder of CNS Loss of dopaminergic neurons (depigmentation) of substantia nigra pars compacta Lewy bodies (intracellular eosinophillic inclusions-alpha synuclein) ``` TRAPS ``` Tremor Rigidity (cogwheel) Akinesia Postural instabililty Shuffling gait ```

Answer 7

Auto dom. CAG repeat on chromosome 4. Onset b/w 20 and 50 Choreiform movements, aggression, depression, dementia Incr. Dopamine, decr. GABA, Decr. ACh Neuronal death via NMDA-R binding and glutamate toxicity Atrophy of caudate nuclei disrupts BG pathways leading to unwanted movement. Atrophy of caudate w/ ex vacuo dilatation of frontal horns.

Answer 8

Aphasia=higher order inability to speak (language deficit) dyarthria=motor inability to speak Broca=nonfluent aphasia with intact comprehension and impaired repetition (brocas area in inferior frontal gyrus of frontal lobe=language production) Wernicke=fluent aphasia w/ impaired comprehension and repetition (Wernickes area is superior temporal gyrus of temporal lobe=language interpretation/analysis) Conduction=Poor repetition, but fluent speech, intact comprehension (Arcuate fasciculus) Global=nonfluent aphasia w/o comprehension, poor repetition (arcuate, wernickes, broca) Transcortical motor=nonfluent aphasia with good comprehension and intact repetition (area around broca) Transcort. sensory=poor comprehension w/ fluent speech and intact repetition (area around wernickes) Mixed transcorticals=poor comprehension and influent speech but intact repetition (areas around wernickes and areas around brocas)

Answer 9

Disinhibited behavior (hyperphagia, hypersexuality, hyperorality) Amygdala (bilateral) HSV-1

Answer 10

Frontal lobe

Answer 11

Non dominant parietal temporal cortex

Answer 12

agraphia, acalculia, finger agnosia, and left-right disorientation Dominant parietal temporal cortex

Answer 13

Reticular activating system (midbrain)

Answer 14

confusion, opthalmoplegia, ataxia Memory loss, confabulation, personality changes Thiamine deficiency and EtOH use Mammilary bodies (bilateral)

Answer 15

Bilateral hippocampus No new memories

Answer 16

Paramedian pontine reticular formation (PPRF)

Answer 17

Frontal eye fields

Answer 18

Between ACA/MCA and MCA/PCA. Severe hypotension Upper leg/upper arm weakness (ACA/MCA) Defects in higher order visual processing (MCA/PCA)

Answer 19

Vertebral arteries come off the subclavian. They both give of Posterior inferior cerebellar arteries They both give off anterior spinal arteries which join together and head down the spinal cord. They join together to form the basilar artery (at pons) Just as they join together, they give off ant. inf. cerebellar arteries The basilar artery travels along the pons giving off pontine branches At the end of the pons, it gives off Superior Cerebellar arteries It then splits into two posterior cerebral arteries The PCAs give off posterior communicating arteries The interal carotids break off from the common carotid They give off arteries which anastomose with PComs They give off anterior cerebral arteries The ACAs have an anterior communicating artery. The ICAs give off an anterior choroidal artery It then becomes the middle cerebral artery The middle cerebral artery gives off lenticulostriate arteries

Answer 20

Leg=medial Arm=less medial Face=most lateral

Answer 21

PCO2 (incr. PCO2 leads to incr. cerebral blood flow) In extreme hypoxia (<50mmHg), decr. PO2 will cause perfusion to increase In acute cerebral edema, hyperventilation can lead to Decr. PCO2 leading to decr. cerebral blood flow In panic attacks, decr. PCO2 can lead to decr. blood flow leading to fainting

Answer 22

Cerebral perfusion pressure=MAP (blood pressure) - ICP (intracranial pressure) If BP is decr. or ICP is incr., it can reach zero which will result in brain death (no perfusion)

Answer 23

motor cortex-lateral sensory cortex-lateral Temporal lobe MCA

Answer 24

Motor cortex-medial Sensory cortex-medial ACA

Answer 25

Striatum, internal capsule Lenticulostriate Lacunar infarcts (2nd to unmanaged hypertension)

Answer 26

Lateral corticospinal tract Medial lemniscus Caudal medulla-hypoglossal nerve ASA Often bilateral Medial medullary syndrome: infarct of paramedian branches of ASA and vertebral arteries.

Answer 27

Lateral medulla: vestibular nucl, lateral spinothalamic, spinal trigeminal nucl, nucl ambiguus, sympathetic fibers, inferior cerebellar peduncle PICA ``` Lateral medullary (wallenberg) syndrome Nucleus ambiguus effects (dysphagia/hoarseness) are unique to PICA ``` Don't PickA horse that can't eat

Answer 28

Lateral pons: CN nuclei (vestibular nuclei, facial nucleus, spinal trigeminal nucl, cochlear nuclei), symp. fibers Middle and inferior cerebellar peduncles AICA Lateral pontine syndrome Facial nucleus effects unique to AICA

Answer 29

Occipital cortex, visual cortex PCA

Answer 30

Pons, medulla, lower midbrain, corticospinal and corticobulbar tracts, ocular CN nuclei, PPRF Basilar

Answer 31

Aneurysm (saccular) impinges CNs ACom

Answer 32

Saccular aneurysm Eye is down and out with ptosis and mydriasis PCom

Answer 33

Abnormal dilation of artery due to weakening of vessel wall Bifurcations in the circle of willis (ACA and ACom) Rupture-->SAH or hemorrhagic stroke Bitemporal hemianopia via compression of optic chiasm ADPKD, Ehler Danlos Advanced age, hypertension, smoking, blackness CHARCOT ``` Chronic hypertension Small Vessels (BG and thalamus) ```

Answer 34

Neuropathic pain due to thalamic lesions. Initial paresthesias followed in weeks to months by allodynia and dysesthesia. 10% of stroke pts

Answer 35

Rupture of middle meningeal artery after fracture of temporal bone. Lucid interval. Rapid expansion on systemic pressure leading to transtentorial herniation and CNIII palsy biconvex, hyperdense blood collecction does not cross suture lines Cross falx, tentorium

Answer 36

Rupture of bridging veins Slow venous bleeding (develops over time) Elderly, alcoholics, blunt trauma, shaken baby Crescent shaped hemorrhage Crosses suture lines Midline shift Doe not cross falx, tentorium

Answer 37

rupture of an aneurysm or AV malformation Rapid time course WHOML Bloody or yellow spinal tap Risk of vasospasm due to blood breakdown (not visible on CT=nimodipine) risk of rebleed (visible on CT) 2-3 days later

Answer 38

systemic hypertension Amyloid angiopathy, vasculitis, neoplasm BG and internal capsule Can be lobar

Answer 39

Irreversible damage after 5 min. of hypoxia Hippocampus, neocortex, cerebellum, watershed areas Noncontrast CT to exclude hemorrhage (before tPA given) CT detection after 6-24 hrs Diffusion weighted MRI within 3-30 min. ``` 12-48 hours=red neuron 24-72 hrs=necrosis + neutro 3-5 days=microglia 1-2 weeks=reactive gliosis + vasc. prolif >2 weeks= glial scar ```

Answer 40

Intracerebral bleeding Hypertension, angicoag, cancer, ischemic stroke followed by reperfusion BG

Answer 41

Acute blockage of vessels leads to ischemia leading to liquefactive necrosis Thrombotic-clot forming directly at site f infarction (MCA) usually over atherosclerosis Embolic: another part of body. Multiple vasc. territories. A fib/paradoxical emboli Hypoxic: hypoperfusion or hypoxemia; all watershed areas; CV surgeries Treatment: tPA (within 3-4.5 hr f nset and no hemorrhage), reduce risk w/ aspirin/clopidogrel; optimum conrtrol of BP, Blood sugars, lipids; treat conditions that increase risk (a fib, DVT)

Answer 42

Brief reversible episode of focal neuro dysfunction w/o acute infarction (neg. MRI), with the majority resolving in < 15 minutes. Deficits due to focal ischemia.

Answer 43

Large venous channels that run through the dura. Drain blood from cerebral veins and receive CSF from arachnoid granulations. Empty into jugular vein. Mainlocation of CSF return.

Answer 44

Ependymal cells of choroid plexus make CSF. Lateral ventricle to the foramina of Monro to the 3rd ventricle to the cerebral aqueduct of sylvius to the 4th ventricle to the subarachnoid space via foramen of Lushka (lateral) and foramen of magendie (medial). It is then reabsorbed by arachnoid granulations which drain into dural sinuses.

Answer 45

Pseudotumor cerebri Incr. ICP w/ n apparent cause on imaging Headaches, diplopia (CNVI palsy), no mental status alteration. Papilledema Worman of childbearing age, vitamin A excess, danazol Lumbar puncture=incr. opening pressure and provides headache relief Weight loss, acetazolamide, topiramate, invasive procedures.

Answer 46

Decr. CSF absorption by arachnoid granulations Incr. ICP, papilledema, herniation Arachnoid scarring post meningitis

Answer 47

Elderly Idiopathic CSF pressure elevated only episodically No result in subarachnoid space volume Expansion of ventricles distorts the fibers of the corona radiata Urinary incontinence, ataxia, cognitive distortion wet, wobbly, and wacky

Answer 48

Caused by structural blockage of CSF circ. within ventricular system

Answer 49

Appearance of incr. CSF on imaging, but actually due to decr. brain tissue Alzheimers, advanced HIV, Pick disease ICP normal Triad not seen.

Answer 50

Precentral gyrus and anterior part of paracentral lobule Corona radiata to posterior limb of internal capsule (b/w thalamus and globus pallidus Int. capsule to cerebral crus (inferior and superior colliculus (midbrain)) Cerebral crus to basilar part of pons To pyramid (medulla) to pyramidal decussation (caudal third of medulla) to lateral corticospinal tract (spine) (post. part of lateral funiculus) some fibers do not cross and stay in anterior funniculus CORTICOBULBAR Descends in much the same manner, but in pons and medulla, the fibers become much more diffuse and thus a single lesion is unlikely to have much effect.

Answer 51

Post=cortex anterior=spinal cord flocc=vestibular entire=inferior olive vermis=fastigial paravermis=intermediate lateral=dentate POST Association centers to internal capsule to cerebral crus to pontine nuclei to pontocerebellar tracts to CL middle cerebellar peduncle to posterior lobe to purkinje neurons to dentate nucleus to superior cerebellar peduncle to decussation (near red nucleus) to VL nucleus to motor cortex. ANTERIOR Lower limb to gracile tract to dorsal nucleus or clarke to dorsal spinocerebellar tract to inferior cerebellar peduncle Upper limb to cuneate tract to accessory cuneate nucleus to cuneocerebellar tract to inf. cerebell peduncle to vermis and paravermis to purkinje to interposed and fastigial Fastigial to vestibular nuclei to paravertebral and proximal muscles Interposed to superior cerebellar peduncle to decussation to red nucleus to distal muscles FLOCCULO (equilibrium and eye movements) Vestibular nerve and nuclei to restiform body (medial part of inf .cere. ped.) to flocculo to fastigial to vest. nuclei and reticular formation (all bilateral) Vestibuloocular fibers (from nuclei) to external ocular nuclei (3, 4, 6) Medial and lateral vestibulospinal tracts (anterior funniculus) Mossy fibers to granule cells Inf. Olive=climbing fibers Cortex and red nucleus to principal nucleus Spinal cord to accessory nuclei Olivocerebellar fibers to CL restiform body of inf. cereb. peduncle to all parts of cerebellar cortex as climbing fibers.

Answer 52

below midthoracic to gracile tract Above to cuneate tract Gracile and cuneate tracts to gracile and cuneate nuclei (caudal medulla) to decussation to CL medial lemniscus to VPL of thalamus to posterior limb of int. capsule to postcentral gyrus and posterior part of paracentral lobule

Answer 53

Peripheral ganglia to tract of lissauer (up 1 to 2 segments) to marginal nucleus to ventral white commisure to CL spinothalamic tract (anterior part of lateral funiculus) to VPL to post. limb to sensory cortex.

Answer 54

Trigeminal ganglia to principal sensory nucleus (posterolateral part of pons) to CL trigeminothalamic tract to VPM in thalamus to post. limb of int. capsule to sensory cortex.

Answer 55

Trigeminal ganglion into pons and descend as spinal trigeminal tract where they synapse on caudal part of spinal trigeminal nucleus to CL trigeminothalamic tract to VPM to int. capsule to sensory cortex.

Answer 56

8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal Nerves C1-7 exit above vert. C1-7 C8 exits below C7 and above T1. The rest exit below their corresponding vert Down to L1-L2 Subarachnoid to lower border of vertebra S2 LP at L3-L4 or L4-L5

Answer 57

Nucleus pulposus herniates through annulus fibrosus Posterolateral L4-L5 or L5-S1

Answer 58

Legs are lateral in lateral tracts Dorsal is organized with arms outside and legs inside Corticospinal/spinothalamic (cervical is medial and sacral is lateral) Order is reversed in dorsal columns (gracile internal, cuneate external)

Answer 59

Anterior horns; LMN lesions only Floppy baby with marked hypotonia and tongue fasciculatins Median age of death of 7 months .

Answer 60

White matter of cervical region Random and asymmetric lesions Demyelination Scanning speech Intention tremor Nystagmus

Answer 61

Anterior horn and corticospinal tract UMN and LMN deficits Superoxide dismutase 1 Fasciculations then atrophy and weakness of hands Fatal Riluzole modestly incr. survival by decr. presynaptic glutamate release (riLOUzole)

Answer 62

Only spares dorsal columns and tracts of Lissauer Upper thoracic ASA territory is watershed area.

Answer 63

Dorsal columns and roots tertiary syphilis Demyelination Impaired sensation and proprioceptis which leads to progressive sensory ataxia (can't sense or feel legs leading to poor coordination) Charcot joints, shooting pain, argyll robertson pupils Absence of DTRs and + romberg sign

Answer 64

Syrinx exapnds and damages anterior white commisure (spinothalamic tract) Bilateral loss of pain and temp. (C8-T1) Chiari I malformation

Answer 65

Subacute combined degeneration Demyelination of dorsal columns, lateral corticospinal and spinocerebellar Ataxic gait Paresthesia Impaired position and vibration sense

Answer 66

GAA trinucl. repeat on chrom. 9 Frataxin (9 letters) Impairment in mitochondrial function Friedrich is Fratastic (frataxin); he's your favorite frat brother, always staggering and falling but has a sweet (DM) big heart (hypertrophic cardiomyopathy)

Answer 67

Hemisection of spinal cord Above T1, may have symptoms of Horner syndrome

Answer 68

``` C2 posterior half of skull cap C3 turtle neck C4 low collar shirt T4 at nipple T7 xyphoid process T10 at the umbilicus L1 inguinal ligament L4 knee S2,S3,S4=erection and sensation of penile and anal zones ```

Answer 69

1,2, buckle my shoe 3,4 kick the door 5,6 pick up sticks 7,8 lay them straight 1,2, testicles move 3,4 winks galore S1/2=achilles L3/4=patella C5/6=Biceps C7/8=Triceps L1/2=cremaster reflex S3/4=anal wink reflex

Answer 70

Present in healthy infant, absent in adults Disappear in first year of life Frontal lobe inhibition Frontal lobe lesions Moro reflex: Abduct/extend arms when startled then draw together rooting reflex: Movement of head toward one side if cheek or mouth is stroked sucking reflex:Sucking response when roof of mouth is touched palmar reflex: Curling of fingers when palm is stroked plantar reflex: Dorsiflexion of large toe and fanning of others with plantar stimulation galant reflex: Stroking along one side of spine when in ventral position causes lateral flexion of lower body toward stimulated side

Answer 71

Conjugate vertical gaze center Auditory Paralysis of vertical gaze center due to lesion in superior colliculi

Answer 72

Sensory=alar plate=lateral motor=basal plate=medial

Answer 73

CN I=cribiform Middle=sphenoid bone=CN II-VI Optic canal=CNII, opthalmic artery, central retinal vein Superior orbital fissure=CNIII, IV, V1, VI, opthalmic vein, sympathetic fibers Foramen rotundum=CNV2 Foramen Ovale=CNV3 Foramen Spinosum=Middle mening artery CNV exit Standing Room Only Posterior=temporal or occipital Internal auditory meatus=CN VII, VIII Jugular foramen=CNIX, X, XI, jugular vein Hypoglossal canal=CNXII Foramen magnum=spinal roots of CNXI, brain stem, vertebral arteries.

Answer 74

Olfactory=smell (no thalamic relay) Optic=sight Oculomotor=eye movement, pupillary constriction, accomodation, eyelid opening Trochlear=eye movement Trigeminal=mastication (V3), facial sensation (V1-V3), somatosensation from anterior 2/3 of tongue Abducens=eye movement Facial=Facial movement, taste from anterior 2/3 of tongue, lacrimation, salivation (submand. and subling, not parotid, though it courses through), eyelid closing, stapedius muscle in ear Vestibulocochlear=hearing, balance Glossopharyngeal=Taste and somatosensation from posterior 1/3 of tongue, swallowing, salivatin (parotid), monitoring carotid body and sinus, stylopharygeus muscle (elevates pharynx/larynx) Vagus=Taste from epiglottic region, swallowing, soft palate elevation, midline uvula (pulls it), talking, coughing, thoracoabdominal viscera, monitoring aorta arch chemo/baro receptors Accessory=Head turning/shoulder shrugging Hypoglossal=tongue movement

Answer 75

Visceral sensory info (taste, baroreceptors, gut distention)=VII, IX, X Moter innervation of pharynx, larynx, upper esophagus=IX, X, and XI Dorsal motor nucleus=autonomic (parasym) fibers to heart, lungs, upper GI=X

Answer 76

``` Corneal=V1 opthalmic, VII Lacr=V1, VII Jaw Jerk=V3, V3 Pupillary=II, III Gag=IX, X ```

Answer 77

Jaw deviates to side of lesion (lateral pterygoid) Uvula deviates away from lesion, weak side palate collapses Weakness turning head to CL side of lesion (SCM) Shoulder droop on side of lesion Tongue deviates to side of lesion.

Answer 78

Blood rom eye and superficial cortex to cavernous sinus to dural sinuses to internal jugular vein. CNIII, IV, V1, maybe V2, VI, postganglionic sympathetic pupillary fibers, ICA Variable opthalmoplegia (VI most sensitive), decr. corneal sensation, Horner syndrome, maybe decr. maxillary sensaiton Pituitary tumor mass effect Carotid/cavernous fistula Cavernous sinus thrombosis (infection)

Answer 79

Visible portion of the ear (pinna), auditory canal and eardrum. Transfers soundwaves via vibration of ear drum

Answer 80

air filled space with three bones called the ossicles (malleus, incus, stapes). Conduct and amplify sound from eardrum to inner ear

Answer 81

Snail shaped fluid filled cochlea w/ basilar membrane that vibrates secondary to sound waves. Vibration transduced via specialized hair cells leading to auditory nerve signaling to brain stem. Low frequency at apex near helicotrema High frequency at base of cochlea

Answer 82

Conductive: R=Abnormal (bone > air) W=to affected ear Sens: R=Normal (air > bone) W=To unaffected ear Damage to stereociliated cells in organ of corti. Loss of high frequency first. Sudden extremely loud noises produce hearing loss due to tympanic membrane rupture

Answer 83

Overgrowth of desquamated keratin debris within middle ear space Erode ossicles and mastoid air cells leading to conductive hearing loss

Answer 84

UMN=CL paralysis of lower face LMN=IL paralysis of whole face Destruction of facial nucleus or nerve LMN lesion Idiopathic=bells palsy Gradual recovery usually Lyme disease, HSV, VZV, sarcoidosis, tumors, diabetes Corticosteroids

Answer 85

Masseter, temporalis, medial pterygoid Lateral pterygoid V3

Answer 86

Ciliary epithelium (beta 2) in vitreous chamber Then to posterior chamber (infront of lens, behind iris) then to anterior chamber (in front of lens and iris) Trabecular meshwork to canal of schlemm Ciliary muscle contraction can help open trabecular meshwork. Pupillodilator muscle contraction can close the angle even more.

Answer 87

Optic disc atrophy with characteristic cupping (thinning of outer rim of optic nerve head vs. normal), elevated ICP, and prog. periph. visual field loss Incr. age, afr. american, FH Painless Primary=unclear Secondary=blocked trabecular meshwork from WBCs (uveitis), RBCs (vitreous hemorrhage), retinal elements (retinal detachment) Primary=enlargement or forward movement of lens against central iris which leads to obstruction of normal aq. humor which leads to fluid build up behind iris which pushes it forward and impedes flow into trabecular meshwork Secondary=hypoxia from retinal disease (DM, vein occusion) induces vasoproliferatin in iris that contracts angle Chronic=asymptomatic w/ damage to optic nerve and periph. vision True ophthalmic emergency IOP pushes iris forward, abrupt angle closure Very painful, red eye, sudden vision loss, halos around lights, rock hard eye, frontal headache NO EPI (mydriasis)

Answer 88

common cause of impaired vision, correctable w/ glasses Hyper: eye too short for refractive power of cornea and lens (light focused behind retina)=farsightedness Myopia: eye too long for refr. power of cornea and lens (light focused in front of retina)=nearsighted AStigmatism: abnormal curvature of cornea leads to different refractive power at different axes Presbyopia: Age related impaired accomodation, possibly due to decr. lens elasticity (reading glasses)

Answer 89

Painless, often bilateral opacification of lens Decrease in vision Incr. age, smoking, EtOH, excessive sunlight, prolonged corticosteroid use, classic galactosemia, galactokinase defic, DM, trauma, infection

Answer 90

Iris and choroid (ant. and post) Inflammation of uvea Hypopyon (accumulation of pus in ant. chamber) Conjuctival redness Systemic infl. disorders=sarcoid, RA, HLA B27 conditions

Answer 91

Degeneratin of macula. Causes distortion (metamorphopsia) and eventual loss of central vision (scotomas) Yellowish EC material with gradual decr. in vision Prevent progression w/ MV and antioxidant supplemetns Rapid loss of vision (bleeding from neovasc) Anti VEGF injections or laser

Answer 92

Retinal damage due to chronic hyperglycemia Non-prolif=damaged capillaries leadk blood, lipids and fluid seep into retina, macular edema Blood sugar control, macular laser Prolif=hypoxia to neovasc to traction on retina Peripheral retinal photocoag, Anti VEGF

Answer 93

Nearby arterial atherosclerosis | Retinal hemorrage, vein engorgement, edea in affected area

Answer 94

Separation of neursensory layer of retina from outermost pigmented epith (shields excess light, supports retina) Degentartion of photorecep to vision loss retinal breaks, diabetic traction, infl. effusions Splaying and paucity of retinal vessels High myopia Flashes, floaters then monoocular loss of vision Surgical emergency

Answer 95

Acute painless monocular vision loss Retina cloudy with atten vessels and cherry red spot at fovea Inherited retinal degen Painless, progressive vison loss beginning w/ night blindness Bone spicule shaped deposits around macula Retinal edema and necrosis leading to scar CMV, HSV, VZV Immunosuppression Optic disc swelling de to incr. ICP Enlarged blind spot and elevated optic disc with blurred margins on fundoscopic exam

Answer 96

Parasympathetic Light in either retina sends signal to pretectal nuclei in midbrain that activates bilateral edinger westphal nuclei Pupils conctract bilaterally

Answer 97

Sympathetic 1st neuron: Hypothalamus to ciliospinal center of budge (C8-T2) 2nd: exit at T1 to superior cervical ganglion (near lung apex, subclavian vessels) 3rd: Plexus along internal carotic through cavernous sinus; enters orbit as long ciliary nerve to pupillary dilator muscles Also innervate smooth muscles of eyelids (minor retractors) and sweat glands of forehead and face.

Answer 98

Optic nerve damage or severe retinal injury leasd to decr. bilateral pupillary constriction when light is shone in affected eye relative to other eye Swinging flashlight test

Answer 99

Ptosis, anhidrosis, miosis Damage to sympathetic system to eye. Lesion of spinal cord above T1 (pancoast tumor, brown sequard syndrome, late stage syringomyelia) or any interruption in the pathway.

Answer 100

CNIII has motor (central) and parasymp (peripheral) Motor=IR, IO, MR, SR Parasymp: Pupillodilation ``` Motor=Ptosis, down and out gaze Vascular disease (DM) due to decr. diffusion of oxygen and nutrients to interior fibers. ``` Para: Diminished pupillary light reflex, mydriasis, maybe down and out gaze Compression (PCom aneurysm, uncal herniation)

Answer 101

Innervate superior oblique: abducts, intors, and depresses while adducted. Eyes move upward, particularly w/ CL gaze Head tilt toward the side of the lesion

Answer 102

LR Medially directed eye that cannot abduct

Answer 103

Upside down and left-right reversed Optic nerve to optic chiasm (near stalk of pituitary=middle of chiasm and ICAs=lateral chiasm Optic tract passes Posterolateral along hypothalamus and cerebral crus to synapse on LGN, though some bypass LGN to superior colliculus (pretectal nuclei/miosis). LGN receives ips. and CL fibers containing info from CL visual field. From LGN, into post limb of int caps to optic radiation Optic radiation spreads into dorsal (through parietal lobe) and ventral fibers/meyers loop (through temporal) Contained in dorsal loop is the inf. visual field Contained in ventral loop is the superior visual field Optic radiation terminates in the calcarine sulcus (medial surface of the occipital lobe) which is the visual or striate cortex.

Answer 104

Right anopia: right optic nerve bitemporal hemianopia (causes): medial optic chiasm (pituitary lesion) Left homonymous hemianopia: right optic tract left upper quadrantic anopia (causes): Right meyers loop (MCA, temporal lobe) left lower quadrantic anopia (causes): Right dorsal optic radiation (MCA, parietal) Left hemianopia with macular sparing (causes): Right cortex (PCA) Central scotoma (causes): Macula (macular degeneration)

Answer 105

Pair of tracts that allow for crosstalk b/w CNVI and CNIII nucle. It coordinates both eyes to move in same horizontal directin. HIghly myelinated (quick). When looking left, left CNVI (LR) stimulates right CNIII (MR) so they both look left. Unilateral or bilateral (MS) Internuclear Opthalmoplegia (INO). CNVI makes the left eye look left, but since the right MLF is injured, the right eye doesn't look left. Also, the CNVI overfires causing nystagmus in left eye. Convergence is normal. Right INO=right paralyzation (Right MLF).

Answer 106

voluntary conjugate eye movements eyes turn to CL side.

Answer 107

A decr. in cognitive ability, memory, or function w/ intact consciousness

Answer 108

Older people. DS E2 decr. risk; E4 incr. risk APP, Presenelin 1, 2 incr. risk of early onset Widespread cortical atrophy; narrowing of gyri and widening of sulci. Senile plaques in gray matter made up of EC beta amyloid core (from APP). Amyloid angiopathy can lead to IC hemorrhage Neurofibrillary tangles: intracellular, flame shaped, hyperphosphorylated tau protein->insoluble cytoskeletal elements.

Answer 109

Dementia, aphasia, parkinsonian aspects; change in personality Frontotemporal dementia (spares parietal lobe and post. 2/3 of sup. temp. gyrus). Pick bodies: silver staining spherical tau protein aggregates Frontotemporal atrophy

Answer 110

Initially dementia and visual hallucinations, then parkinsonian. Lewy bodies in cortex (alpha synuclein)

Answer 111

Rapidly progerssive (weeks to months) dementia with myoclonus (startle myoclonus). Spongiform cortex Prions (PrPc (alpha) to PrPsc (beta pleated sheat))

Answer 112

Multi-infarct/vascular Syphillis HIV Vit. B1, 3, or 12 defic. Wilson Disease Normal pressure hydrocephalus

Answer 113

Autoimmune inflammation and demyelination of CNS (brain and spinal cord)=IgG to Oligodendroglia ``` Optic neuritis (sudden loss of vision and marcus gunn pupils) INO Hemiparesis Hemisensory symptoms Bladder/bowel incontinence Scanning speech (broken into syllables) Intention tremor Nystagmus ``` Women in their 30s and 20s Whites living further form the equator Incr. protein (IgG) in CSF Oligoclonal (IgG) bands are diagnostic MRI is gold standard: Periventricular plaques (areas of oligodendroctye loss and reactive gliosis) with destruction of axons; Multiple white matter lesins separated in space and time. Slow progression w/ disease modifying therapies (Beta interferon, natalizumab) Acute flares with IV steroids Symptomatic treatment for neurogenic bladder, spasticity, and pain

Answer 114

Acute inflammatory demyelinating polyradiculopathy Autoimmune, destroys schwann cells Inflammatin and demyelination of periph nerves and motor fibers Symmetric ascending muscle weakness/paralysis Possible autonomic dysreg (cardiac, hypertension, hypotension) Possible sens. abnormalities Almost all survive Majority recover completely after weeks t months Incr. CSF protein w normal cell count Incr. protein may cause papilledema Infections (C. jejuni, viral): molecular mimicry inoculations stress Resp. support plasmapheresis, IVIG

Answer 115

Multifocal periventricular inflammation and demyelination after infection (commonly measles or VZV) or certain vaccines (rabies/smallpox) Hereditary (auto dom) Motor and Sensory Neuropathy. Group of progressive nerve disorders related to defective production of proteins involved in structure and function of periph nerves of myelin sheath. Scoliosis and foot deform (high or flat arches) Auto recessive LSD caused by defic of galactocerebrosidase leading t buidl up of galactocerebroside and psychosine which destroys the myelin sheath. Periph. neuro., devel. delay, optic atrophy, globoid cells Auto recess. LSD due to arylsulfatase A defic. leading to build up of sulfatides leading to impaired production and destruction of myelin sheath leading to central and periph demyelinatin with ataxia, dementia. Demyelination of CNS due t destruction of oligodendrocytes. JC Virus. 2-4% of AIDS patients (remains latent). Rapidly progressive, usually fatal. Natalizumab, rituximab

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X linked. disrupted metab. of VLCFAs leading to excess build up in nervous ystem, adrenal gland, and testes. Progressive disease that can lead to long term coma/death and adrenal gland crisis.

Answer 117

Synchronized, high frequency neuronal firing A disorder of recurrent seizures Continous or recurring seizures that may result in brain injury (>10-30 min.) Children=genetics, infection (febrile), trauma, congential, metabolic Adults=tumor, trauma, stroke, infection elderly=stroke, tumor, trauma, meta\bolic, infection

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Single area of brain Medial temporal lobe Seizure aura Can generalize Consciousness intact (motor, sensory, autonomic, psychic) Impaired consciousness

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Diffuse. Absence=petit mal=3Hz, no postictal confusion; blank stare Myoclonic=quick, repetitive jerks tonic-clonic=grand mal=alternating stiffness and movement tonic=stiffening atonic=drop seizures

Answer 120

Pain due to irritation f structures such as the dura, cranial nerves, or extracranial structures. ``` CLUSTER Unilateral 15 min.-3hr.; repetitive Repetitive brief headaches, excruciating periorbital pain with lacrimation and rhinorrhea. May induce horner syndrome. More common in males 100% O2, sumatriptan ``` TENSION bilateral >30 min. (usual 4-6 hr.), constant STeady pain. No photophobia, phonophobia, or aura Analgesics, NSAIDS, acetaminophen; amytriptyline for chronic pain MIGRAINE Unilateral 4-72 hr. Pulsating pain with nausea, photophobia, or phonophobia. Aura. Irritation of CNV, meninges, or blood vessels Abortive therapies (triptans, NSAIDS) and prophylaxis (propanolol, topiramate, Ca channel blockers, amytriptyline) SAH, meningitis, hydrocephalus, neoplasia, arteritis Trigeminal neuralgia (repetitive shooting pain in distributin of CN V.

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Sensation of spinning while actually stationary Periph=Inner ear etiology. Positional testing-->delayed horizontal nystagmus Central=brain stem or cerebellar. Directional change of nystagmus, skew deviation, diplopia, dysmetria. Positional testing-->immediate nystagmus in any directioin. Focal neuro findings.

Answer 122

Congenital, non inherited, dvelopmental anomaly of neural crest derivatives due to activating mutation of GNAQ. Small blood vessels Port-wine stain on the face Ipsi leptomeningeal angioma leading to seizures/epilepsy Intellectual disability episcleral hemangioma--->early nset glaucoma

Answer 123

``` Hamartomas in CNS and skin Angiofibromas Mitral regurg Ash-leaf spots Rhabdomyoma (cardiac) Dominant (autosomal) Mental retardation Angiomyolipoma (renal) Seizures Shagreen patches Incr. incidence of subependymal astrocytomas and ungual fibromas ```

Answer 124

Mutated NF1 tumor suppressr gene (neurofibromin, a neg. regulator of RAS) on chrom. 17 Von Recklinghausen Neural crest deriv Cafe Au lait spots Lisch nodulse Cutanoeus neurofibromas Optic gliomas, pheochromocytomas

Answer 125

Hemangioblastomas (high vasc. w/ hyperchromatic nuclei) in retina, brain stem, cerebellu, and spine Angiomatosis (cavernous hemangiomas kin skin mucosa, organs) Bilateral RCC Pheochromocytomas

Answer 126

INflammation of the leptomeninges (pia and arachnoid) Neonates=group b strep, e coli, listeria Children=N. meningitidis (nasopharyngeal to blood) Adults/elderly=Strep pneumo Non vaccinated=H. influenze Children=cocsackievirus Immun=fungi Headache, nuchal rigidity, and fever Photophobia, vomiting, and altered mental status may be present Lumbar puncture Bacterial: Neutrophils w/ decr. CSF glucose, possible gram stain and culture Viral: Lymphocytes w/ normal CSF glucose Fngal: Lymph. w/ decr. CSF glucose Complications with bacterial: Death:herniation due to edema Hydrocephalus, hearing loss, and seizures due to fibrosis.

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Lung, breast, kidney Multiple, well circumscribed lesions at the gray white junction Accordig to cell type of origin Adult=supratentorial Glioblastoma multiforme, meningioma, schwannoma Children=infratentorial Pilocytic astrocytoma, ependymoma, and medulloblastoma

Answer 128

High grade, malignant astrocytes Most common malig CNS tumor in adults Cerebral hemisphere and crosses corpus collosum (butterfly) Regions of necrosis surrounded by tumor cells (pseudopalisading) and endothelial cell prolif. GFAP positive Poor prognosis

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Benign tumor of arachnoid cells Most common benign CNS in adults More common in women; not likely in children Seizure: tumor compresses but does not invade cortex Round mass attached to dura Whorled pattern; psammoma bodies

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Benign tumor of schwann cells Cranial or spinal nerves; in cranium, CNVIII at cerebellopontine angle Loss of hearing, tinnitus S-100 positive NF2=bilateral CNVIII schwannomas

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Malignant tumor of oligodendrocytes Calcified tumor in the white matter, usually frontal lobe seizures, maybe fried egg appearance

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Benign tumor of astrocytes Most common CNS tumor in children Cerebellum Cystic lesion with a mural nodule Rosenthal fibers (thick eosinophilc processes of astrocytes) and eosinophilic granular bodies GFAP

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Malignant tumor from granular cells of cerebellum (neuroectoderm) Children Small, round blue cells; Homer-Wright rosettes Poor prognosis Grows rapidly, spreads via CSF Metastasis t cauda equina

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Malig tumor of ependymal cells Children 4th ventricle hydrocephalus Perivascular pseudorosettes

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Epithelial remnants f rathkes puch Supratentorial mass in chldren or teens Compress optic nerve; bitemporal hemianopsia Calcifications on imaging Benign, but recurs after resection.

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Can compress ACA Caudal displacement of brainstem leading to rupture of paramedian basilar artery branches leading to duret hemorrhages, usually fatal. Uncus=medial temporal lobe Compresses CNIII, ipsilateral PCA, CL crus cerebri at kernohan notch (ipsi paresis) Coma and death result when these herniations compress brain stem.