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Step 1 12.4.12
Neuro II
| Question | Answer |
|---|---|
| What normally drives cerebral perfusion? When does it change? | normally driven by PCO2, but also PO@ with severe hypoxia (hypoemia incr CPP only if pO2<50mm Hg) |
| What is a useful measure to lower ICP in cases of acute cerebral edema (stroke, trauma)? | therapeutic hyperventilation ( decr pCO2) |
| What composes the anterior cicrulation of the circle of Willis? What is it derived from? | derived from internal carotid:ACA, lateral striate, MCA |
| What composes the posterior circulation of the circle of Willis? From what is it derived? | derived from subclavian: AICA, ASA, basilar, PICA, PCA, vertebral a. |
| What 4 important areas does the MCA supply? | motor cortex- upper limb and face. sensroy cortex- upper limb and face, Wervicke's area, Broca's area |
| What Sx are seen in a stroke of MCA? | contralateral paralysis and contralateral loss of sensation of upper limb and face. can see hemineglect affects nondominant(right) side |
| What 2 areas does the ACA supply? | motor cortex- lower limb. sensory cortex- lower limb |
| What Sx are seen in a stroke of ACA? | contralateral paralysis and contralateral loss of sensation in lower limb |
| What 2 areas does the lateral striate artery supply? | striatum, internal capusle |
| what sx are expected in a stroke of the lateral striate artery? | contralateral hemiparesis/hemiplagia |
| What artery do lacunar infarcts most commonly affect and what is a common setting for them? | usually affects lateral striate artery. these happen secondary to unmanaged hypertension |
| What 3 areas does the ASA supply? | lateral corticospinal tract, medial lemniscus, caudal medulla-hypoglossal nerve |
| What Sx are expected in a stroke of the ASA? | contralateral hemiparesis of lower limbs, decr contralateral proprioception, ipsilateral hypoglossal dysfunction (tongue deviates ipsilaterally) |
| Which way does the tongue deviate in a lesion of the hypoglossal nerve at ASA? | ipsilaterally |
| What important areas does PICA supply? | 1. lateral medulla = vestibular nuclei, lateral spinothalamic tract, spinal trigeminal nucleus, nucleus ambigguus, sympathetic fibers. 2. Inferior cerebellar peduncle |
| What Sx are associated with a stroke of PICA? | 1. vomiting, vertigo, nystagmus 2. decr paint and temp in limbs and face 3. dysphagia and hoarseness, decr gag reflex 4. Ipsilateral HOrner's syndrome 5. ataxia, dysmetria |
| Where is the stroke in lateral medullary "Wallenber's) syndrome? | PICA |
| Effects on what nucleus are specific to PICA? | nucleus ambiguus |
| Hoarseness and dysphagia are specific to what lesion? | PICA |
| What important areas does AICA supply? | 1. Lateral pons= vestibular nuceli, facial nucleus, spinal trigeminal nucleus, cochlear nuclei, sympathetic fibers 2. middle and inferior cerebellar peduncles |
| What sx are associated with a stroke of AICA? | 1.vomiting, vertigo, nystagmus 2. paralysis of face, decr lacrimation and salivaton 3. decr taste in anterior 2/3 of tongue 4. decr corneal reflex 5. decr pain and temp in face 6. ipsilateral hearing loss 7. ipsilateral Horner's syndrome |
| A stroke in what artery is suggested by lateral pontine syndrome? | AICA |
| Facial nucleus effect such as facial droop are specific to a stroke where? | AICA |
| What important areas does PCA supply? | occipital cortex, visual cortex |
| What Sx would be associated with a stroke of PCA? | contralateral hemianopsia with macular sparing |
| What locations are berry aneurysms often found? Which one could cause inpingment on cranial nerves? | AComm, PComm. both can impinge on cranial nerves |
| Where would you suspect a berry aneurysm to be if visual field defects are seen? | Acomm. these lesions are aneurysms not strokes |
| Where would you suspect a berry aneurysm to be if CN III palsy is seen (eye is down and out)? | PComm, lesions are aneurysms, not strokes |
| What is the most common site for a berry aneurysm? | bifurcation of the anterior communicating artery |
| What happens if a berry aneurysm ruptures? | hemorragic stroke/subarachnoid hemorrhage |
| What other conditions are assoicted with predisposition for berry aneurysms? | ADPKD, Ehlers-Danlos syndrome, Marfan's syndrome |
| What are some major RF for berry aneurysm? | advanced age, HTN, smoking, higher risk in AA |
| What are Charcot-Bouchard microaneurysms? | associated with chronic HTN, affects amll vessels in basal ganglia and thalamus typically |
| What causes an epidural hematoma and what is the interval? | rupture of middle meningeal artery (branch of maxillary) secondary to fracture of temporal bone |
| What is the course of a epidural hematoma? | rapid expansion under systemic arterial P-->transtentorial herniation. CN III palsy |
| What does CT for an epidrual hematoma show? | biconvex disk not crossing the suture lines. can cross the falx, tentorium |
| What causes a subdural hematoma, what is its interval? | rupture of bridging veins. slow venous bleeding so the hematoma develops over time |
| What are some common settings for a subdural hematoma? | elderly, alcoholics, blunt trauma, shaken baby |
| What are some predisposing factors for a subdural hematoma? | brainatrophy, shaking, whiplash |
| What is seen on CT in a subdural hematoma? | crescent chaped hemmorhage. mid line shift, gyri are preserved due to equalized pressures. can't cross the falx or tentorium |
| What causes a subarachnoid hemmorhage? What is its interval? | rupture of an aneurysm (often berry in Marfan's, Ehler's Danlos, ADPKD) or AVM. rapid time course |
| What is the presentation of a subarachnoid hemmorhage? What might be seen in a spinal tap? | pt complains of "worst headache of my life", bloody or yellow (xanthochromic) on ST. |
| What are the major complications of a subarach noid hemmorhage? When do they occur and how do you treat? | 2-3 d afterward. risk of vasospasm due to blood b reakdown treat with nimodipine. can also see rebleed visible on CT |
| What is the cause of intraparencymal hemorrhage? | systemic HTN, but also amyloid angiopathy, vasculitis, neoplasm. |
| Where does an intraparenchymal hemorrhage typically occur? | usually basal ganglia, but can be lobar |
| How long before irreversible damage appears in ischemic brain disease? | 5 minutes |
| What parts of the brain are most vulnerable to ischemic injury? | hippocampus, neocortex, cerebellum, watershed areas. |
| When do red neurons appear post ischemic brain injury? | 12-48 hours |
| When sre necrosis and neutrophils seen in ischemic brain disease? | 24-72 hours |
| When are macrophages seen in ischemic brain disease? | 3-5 days |
| When is reactive gliosis and vascular proliferation seen in ischemic braion disease? | 1-2w |
| When is a glial scar seen in ischemic brain disease? | >2w |
| What is the mech and appearance of atherosclerosis in the brain? | thrombi lead to ischemic stroke with subsequent necrosis. forms cystic cavity with reactive gliosis |
| What is the usual mech of hemorrhagic stroke? | intracranial cleed often due to HTN, anticoagulation, cancer. can be csecondary to ischemic stroke followed by reperfusion due to incr vessel fragility |
| What is the mech and etiologies of ischemic stroke? | emboli block large vessels. can see with afib, carotid dissection, patent formane ovale, endocarditits |
| What is a lacunar stroke? What is its usual etiology? | ischemic stroke of small vessels often secondary to HTN |
| What is the tx for ischemic stroke? When isn't it? | tPA within 4.5 hours (as long as pt presents w/in 3 hours of onset) |
| What is a transient ischemic attack (TIA)? | brief reversible episode of neurologic dysfunction lasting fewer than 24hrs, deficits are due to focal ischemia |
| What does stroke imaging look like on MRI? | bright on diffusion weighted MRI in 3-30 mins and bright for 10 days |
| What does stroke imaging look like on CT? | dark on noncontrast CT in 24 hours. If bright on CT= blood (CONTRAI tPA) |
| Where do venous sinuses run? | dura mater where its meningeal and periosteal layers separate |
| what is the drainage of cerebral veins? | cerebral veins-->venous sinuses-->IJV |
| Where does CSF mainly return to the venous system? | superior sagittal sinus |
| What is the connection between the lateral ventricle and 3rd ventricle? | foramen of Monro |
| What is the connection between the 3rd and 4th ventricle? | cerebral aqueduct |
| What is the connection betwen the 4th ventricle and the subaracnoid space? | Foramina of Luschka=lateral, foramen of Megendie=medial |
| What makes and what reabsorbs CSF? | made by choroid plexus, reabsorbed by venous sinus arachnoid granulations |
| What is the mnemonic for the sx of normal pressure hydrocephalus? What is the mech? | "Wet, Wobbly, wacky". expansion of ventricle distorts fibers of corona radiata and leads to dementia, ataxia, urinary incontinence (reversible dementia in elderly) |
| Does normal pressure hydrocephalus incr the subarachnoid space volume? | NO |
| What is the mech and Sx of communicating hydrocephalus? | decr CSF absorbtion by arachnoid villi, which can lead to incr ICP, papilledema, herniation (arachnoid scarring post meningitis) |
| What is the mech of obstructive ( noncommunicating) hydrocephalus? | caused by structural block of CSF flow withing the ventricular system (ex. stenosis of aqueduct of sylvius) |
| What is hydrocephalus ex vacuo? What are some common settings for it? | appearance of CSF in atrophy (alzheimers, advanced HIV, Pick's disease). ICP normal, triad not seen |
| how many spinal nerves are there? What is the distrobution? | 31: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal |
| Where do the cranial nerves exit the SC? | C1-C7 exit via intravertebral formaina above the corresponding vertebrae, all others exit below |
| What is a vertebral disk herniation and where does it most commonyl occur? | nucleus pulposus herniates through annulus fibrosus) usually occurs b/w L5 and S1 |
| Where does the spinal cord and subarachnoid space extend to in adults? | SC=L1-L2. subarachnoid space= lower border of S2 |
| Where is a spinal tap performed? What structure is there? | L3-L$ or L4-L5. at level of cauda equina |
| What are the 2 parts of the dorsal columns of the SC? What is carried there? | DC= pressure, vibration, touch, proprioception. Fasciculus cuneatus= upper body/extremities. Fasciculus gracilis (lower body and extremities) |
| What is carried in the spinothalamic tract? | pain and tempo |
| What is carried in the lateral corticospinal tract? | voluntary motor |
| Where are leg nerve in the lateral corticospinal tract? | legs are lateral in lateral corticospinal tract |
| How is the dorsal column organized? | hands at lateral sides, legs medial |
| Do ascending tracts croos first or synapse first? | synapse, then cross |
| What does the dorsal column- medial lemniscal pathway carry? | ascending pressure, vibration, touch, proprioceptive info |
| What is the 1st order neuron in the dorsal column- medial lemniscal pathway ? Where is its cell body and how does it ascend? | sensroy nerve ending, cell body in DRG--> enters SC and ascends ipsilaterally |
| What is the 1st synapse in the dorsal column- medial lemniscal pathway ? | ipsilateral nucleus cuneatus or gracillis (medulla) |
| What is the 2nd order neuron in dorsal column- medial lemniscal pathway | decussates in medulla--->ascends contralaterally in medial lemniscus |
| What is the 2nd synapse in the dorsal column- medial lemniscal pathway ? | VPL in thalamus |
| What is the 3rd order neuron in the dorsal column- medial lemniscal pathway ? | sensory cortex |
| What does the spinothalamic tract carry? | ascending pain and temp |
| What is the first order neuron in the spinothalamic tract? where is the cell body? | sensory nerve ending (A delta and C fibers) cell body in DRG--> enters SC |
| What is the first synapse in the spinothalamic tract? | ipsilateral gray matter of SC |
| What is the second order neuron in the spinothalamic tract? | decussates at anterior white commisure-->ascends contralateral |
| What is the second synapse of the spinothalamic tract? | VPL of thalamus |
| Where is the 3rd order neuron of the spinothalamic tract? | sensory cortex |
| What does the lateral corticospinal tract carry? | descending voluntary movement of contralateral limbs |
| What is the 1st order neuron in the lateral corticospinal tract? Where is the cell body? | upper motor neuron: cell body in primary motor cortex-->descends ipsilaterally (thru internal capusle) until decussating at caudal medulla(pyramid)-->descends contralaterally |
| What is the 1st synapse of the lateral corticospinal tract? | cell body of the anterior horn (SC) |
| What is the 2nd order neuron in the lateral corticospinal tract? | lower motor neuron: leaves SC |
| What is the 2nd synapse of the lateral corticospinal tract? | neuromuscular junction |
| What are the key findings in a lower motor neuron lesion? | everything is lowered. except incr fasiculations. less muscle mass, decr muscle tone, decr reflexes, downgoing toes) |
| What are the key findings in an upper motor neuron lesion? | everything up( tone, distal tendon reflexes, toes). see babinski sign, spastic paralysis. clasp knife spasticity |
| When is a positive Babinski sign normal? | infants |
| What is a fasciculation? | muscle twitching |
| What is the damage to the SC seen in poliomyelitis and Werdnig-Hoffman disease? | lower motor neuron lesions only due to destruction of anterior horns; flaccid paralysis |
| What is the damage to the SC seen in multiple sclerosis? | mostly white matter of the cervical region. random and asymmetric lesions due to demyelination; scanning speech, intention tremor, nystagmus |
| What is the damage to the SC seen in ALS? | combined lower and motor neuron deficits with no sensory deficit. both upper and lower motro neurone signs |
| What is the damage to the SC seen in complete occlusion of the Anterior spinal a? | spares dorsal columns and tract of Lissauer; upper thoracic ASA territory is a watershed area, as artery of Adamkiewicz supplies ASA below T8 |
| What is the damage to the SC seen in tabes dorsalis? | tertiary syphilis. degeneration of dorsal roots and dorsal columns, impaired proprioception and locomotor ataxia |
| What is the damage to the SC seen in syringomyelia? | damages anterior white commisure of spinothalamic tract (2nd order neurons). results in bilateral loss of pain and temp (C8-T1), see with Chiari Types 1 and 2. can expand and affect other tracts |
| What is the damage to the SC seen in vit B12 neuropathy, vit E defieciency, Friedrich's ataxia? | subacute combined degenertation. demyelination of dorsal columns laterla corticospinal tracts, ataxic gait, hyperreflexia, impaired position and vibrational sense |
| What is the pathophys of poliomyelitis? | caused by poliovirus, transmitted by the fecal oral route. replicates in the oropharync and small intestine before spreading to the bloodstream to CNS where it leads to destruction of cells in anterior horn leading to LMn destruction |
| What are the Sx of poliomyelitis? | malaise, Ha, fever, nausea, abd pain, AT. LMN lesion signs: weakness and atrophy, fasciulations, fibrillation, hyporeflexia |
| What are the key findings in poliomyelitis? | CSf with lymphocytic pleocytosis with slight elevation of protein (no change in CSF glucose). virus is recovered from stool or throat |
| What is Werdnig-Hoffman disease? | a.k.a infantile spinal muscular atrophy. AutoR. present as floppy baby, tongue fasciluations, death around 7 motnhs. associated with degeration of the anterior horns. LMN involvement only |
| What is the lesion in amyotrophic lateral sclerosis (ALS)? What is the common defect? | associated with both LMN and UMN signs. no sensory, cognitive, or oculomotor deficits (stephen Hawking). caused often by defect in superoxide dismutase 1 (SOD1) |
| What is the common presentation of ALS? | fasciulation and eventualy atrophy, progressive and fatal. |
| What is a possible tx for ALS? How does it work? | riluzole treatment modestly lengthens survival by decreasing presynaptic glutamate release |
| What happens in tabes dorsalis? | degeneration of dorsal columns and dorsal roots due to tertiary syphilis, resulting in imparied proprioception and locomotor ataxia |
| What are some common associations with Tabes dorsalis? | Charcot's joints, shooting (lightning) pain, Argyll robertson pupils ( accomidate but dont react to ligt), absense of reflexes, positive romberf, sensory ataxia at night |
| What is the pathophys of Friedrich's ataxia? | autoR tirnucleotide repeat of GAA in gene for frataxinm. leads to impairment of mitochondria |
| What are the common findings in Friedreich's ataxia? | staggering gait, frequent falling, nystagmus, dysartria, pes cavus, hammer toes, hypertrophic cardiomyopathy ( cause of death) |
| How does Friedrich's ataxia present? | in childhood as kyphosis |
| What is a mnemonic for the presentation of Friedreich's ataxia? | favorite frat(axin) bro: always stumbling, staggering and falling |
| What is Brown-Sequard syndrome? What are the 5 key fidnings? | hemisection of the SC. 1. ipsi UMN signs (CST) below 2. ipsi loss of tactile, proprioception below lesion 3. contra loss of pain and temp (STT) below lesion 4. ipsi loss of all sensation at level of lesion 5. LM signs (flaccid paralysis) at lesion level |
| What happens if Brown Sequard lesion is above T1? | patient can present with Horner's syndrome |
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tjs2123
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