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Week 4 - Neuro > Week 4 - Neuro Diseases / Disorders > Flashcards

Week 4 - Neuro Diseases / Disorders Flashcards

1
Q

stroke

A

cerebral vascular accident (CVA), brain attack, sudden onset focal central nervous system deficit due to vascular causes

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2
Q

transient symptoms with infarct

A

increased stroke risk in following weeks/months, symptom resolution but evidence of infarct on imaging

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3
Q

transient ischemic attack (TIA)

A

transient neuological dysfunction due to focal ischemia in brain, spinal cord, or retina without acute infarction - no evidence on imaging

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4
Q

stroke impact

A

leading cause of disability, often requires chronic care, Hispanic / American Indian / Alaska Native / African American more likely

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5
Q

stroke etiology

A

atherosclerotic, occlusion of cerebral vessesl -> lack of O2 -> neuronal death (4 min after blood cessation)

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6
Q

large vessel stroke - more likely over 45

A

direct thrombosis or embolism of cerebral arteries from cervical arteries / aorta / heart

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7
Q

additional causes of large vessel stroke - more likely under 45

A

vasculitis, sickle cell crisis, preeclampsia, vertebral / carotid artery dissection, migraine vasospasm, sympathetic vasospasm (Rx, cocaine, amphetamines)

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8
Q

thrombosis

A

blood clot

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9
Q

embolism

A

intravascular mass from distant site

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10
Q

hemorrhagic stroke

A

hemorrhage leaks into brain tissue

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11
Q

ischemic stroke

A

slot stops blood supply to area of the brain

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12
Q

large vessel ischemic stroke

A

anterior - common carotid -> middle or anterior cerebral arteries; posterior - vertebral artery -> basilar artery -> posterior cerebral artery

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13
Q

small vessel ischemic stroke (lacunar)

A

on penetrating arteries off of cerebral arteries

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14
Q

chronic hypertension and lacunar stroke

A

endothelial injury / tunica media smooth muscle degeneration -> plasma protein deposition -> collagenous fibers -> decreased vessel elasticity; endothelial injury -> platelet aggregation and activated clotting factor -> vessel occlusion

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15
Q

intracerebral hemorrhagic stroke

A

13% of all strokes, most common hemorrhagic stroke, bleeding directly in brain tissue, risk - age / male / hypertension / alcohol / tobacco / diabetes

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16
Q

subarachnoid hemorrhagic stroke

A

bleeding subarachnoid / subdural / epidural space

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17
Q

hypertensive intracerebral hemorrhage (ICH)

A

deep structures of the brain / brainstem / cerebellum, less common on cortex

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18
Q

cortex bleeding

A

associated with mass lesions, vascular malformation, amyloid angiopathy

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19
Q

intracerebral hemorrhage in putamen

A

half of intracerebral bleeds from lenticulostriate branches of middle cerebral artery, symptoms - contralateral hemiparesis (weakness on one side of body), gaze paresis (weakness), aphasia (language disturbance), hemineglect (inability to pay attention to 1/2 visual field)

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20
Q

intracerebral hemorrage in thalamus

A

contralateral hemianesthesia

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21
Q

intracerebral hemorrage in cerebellum

A

vomitting, ataxia, nystagmus, facial paralysis, ipsilateral gaze palsy, decreased level of conciousness

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22
Q

intracerebral hemorrage in pons

A

coma, quadripelgia, pinpoint pupils, autonomic instability

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23
Q

intracerebral hemorrage imaging

A

noncontrast head CT shows large white area

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24
Q

intracerebral hemorrage management

A

surgical removal of clots if supratentorial, stop anticoagulants, possible benefit if lower BP - no benefit steroids / mannitol / glycerol

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25
Q

subarachnoid hemorrhages (SAH)

A

intracraniral vessels between archoid and pia in the subarachnoid space with CSF, often traumatic shear force

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26
Q

non-traumatic subarachnoid hemorrhage

A

aneurysm rupture, 80% spont subarachnoid hemorrhages, 55, men, African Americans, 2-5% of all strokes

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27
Q

subarachnoid hemorrage symptoms

A

severe headache, thunderclap/worst ever, nausea, vomiting, nuchal rigidity, photophobia, altered consciousness, series of small headaches prior to rupture, CN VI or CN III palsy, increased cranial pressure, deficits based on location

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28
Q

anterior cerebral artery aneurysm example

A

bilateral leg weakness

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29
Q

middle cerebral artery aneurysm example

A

hemiparesis (weakness on 1/2 body) or aphasia (language problem)

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30
Q

subarachnoid hemorrhage imaging

A

noncontrast head CT (best within 6 hours when pt is still conscious) - shows lighter diffuse areas or blood pooled in ventricles, lumbar puncture showing blood (xanthochromia or RBC)

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31
Q

subarachnoid hemorrhage management

A

prevent rebleeding, prevent vasospasm, treat neuro complications, nimodipine - Ca channel blocker in CNS dilates small vessels to increase cerebral profusion

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32
Q

subarachnoid hemorrhage surgery

A

bleeding aneurysm, clipped or placement of endovascular coiling device (better outcomes)

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33
Q

subarachnoid hemorrhage risks

A

smoking, hypertension, alcohol, minorities, 1st degree family Hx - aneurysm monitoring, NO association with recurrent headaches or NSAID use

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34
Q

anterior circulation stroke

A

contralateral motor and sensory deficits

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35
Q

middle cerebral artery

A

supplies lateral frontal / parietal / temporal lobes

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36
Q

middle cerebral artery stroke

A

face and arms more affected, homonymous hemianopsia, ipsilateral gaze deviation

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37
Q

dominant cerebral hemisphere stroke

A

usually left side, aphasia (language problems)

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38
Q

nondominant cerebral hemisphere stroke

A

contralateral hemineglect

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39
Q

anterior cerebral artery stroke

A

legs affected, personality changes, rare

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40
Q

ophthalmic artery occlusion

A

amurosis fugax (blindness in one eye), like a shade being drawn

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41
Q

posterior circulation stroke (vertebrobasilar)

A

20% of ischemic strokes

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42
Q

vertebral artery stroke

A

inferior cerebellum and lateral medulla

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43
Q

cerebellar strokes (vertebral artery)

A

vertigo, blurred vision, vomiting, nystagmus, ataxia, postural instability

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44
Q

lateral medullary infarct (Wallenberg syndrome)

A

crossed symptoms, ipsilateral face from cranial nerve damage and contralateral body from ascending afferents that have already crossed over

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45
Q

basilar artery stroke

A

rostral brainstem, occipital lobes, CN palsies, gaze problems, hemianopsia, miosis, altered consciousness (damage to reticular activating system), possible loss of consciousness, 90% mortality

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46
Q

posterior cerebral artery stroke

A

contralateral homonymous hemianopsia, often with macular sparing, possible difficulty naming colors, if nondominant hemisphere - neglect of affected vision field, less obvious type of stroke

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47
Q

small vessel lacunar stroke

A

branches off middle cerebral artery to deep brain = lack of cortical stroke signs (no aphasia, neglects, visual field loss), 5 different stroke syndromes

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48
Q

pure motor lacunar stroke

A

most common lacunar stroke syndrome, infarction of posterior limb of internal capsule, hemiparesis (weakness on 1/2 body) of legs, arms, and face, disruption of descending corticospinal and corticobulbar tracts

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49
Q

pure sensory lacunar stroke

A

infarction of lateral thalamic nucleus, numbness of legs, arms, and face on contralateral side due to disruption of ascending spinothalamic and dorsal column medial lemniscus pathways

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50
Q

time and stroke management

A

critical to determine time last deficit free, pt with ischemic stroke and symptoms for less than 4.5 hrs are candidates for fibrinolytics

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51
Q

stroke and hospitalization

A

acute stroke yes, risk of complications, some transient ischemic attack patients may be outpatient

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52
Q

complications of stroke

A

hemodynamic or respiratory problems, worsening other conditions, psychosocial problems, aspiration, falling, intracranial hemorrhage, cardiac arrhythmia, myocardial infarct, stroke progression

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53
Q

stroke Hx

A

onset, head trauma?, relevant medical Hx and risk factors (atheroscloerosis, heart disease, meds, substances, migraines, seizures, infection, preganancy, trauma), candidate for fibrinolytics?

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54
Q

stroke PE

A

head/neck for signs of seizure/trauma (contusions or tongue laceration), neuro, heart, GI (occult blood if TPA candidate), stroke scale

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55
Q

stroke scale

A

level of consciousness observed / questions / commands, horizontal gaze, visual fields, facial palsy, motor arm, motor leg, limb ataxia, sensory, language, dysarthria, extinction / inattention (neglect)

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56
Q

hemorrhagic stroke imaging

A

noncontrast CT scan

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57
Q

acute / focal ischemic stroke imaging

A

hard to see early changes with noncontrast CT scan, MRI with diffusion weighted imaging good for acute / focal ischemic stroke

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58
Q

vertebrobasilar ischemic stroke imaging

A

magnetic resonance angiography (MRA) or computed tomography angiography (CTA), looks for vascular malformations / aneurysms that can be surgically corrected

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59
Q

stroke labs

A

looks for underlying causes and risk factors, CBC, BMP (basal metabolic panel), hepatic panel, lipid profile, INR (coagulation), EKG (arrhythmia - MI), ultrasound if anterior circulation stroke (came from common carotid with artery stenosis), echocardiogram (ventricular thrombi, valvuvar disease), younger patients (agitated saline echocardiogram - foramen ovale or septal defects)

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60
Q

stroke pts <45, screen for

A

substance abuse, pregnancy, thrombophilias, vasculitis, endocarditis, cervical artery dissection, migraines, hypertension, sickle cells disease, CNS infection, cerebral venous thrombosis, paradoxical embolism, premature atherosclerosis

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61
Q

stroke care

A

observed for neurologic decline, supportive care, maintain normal volume and blood glucose, PT or speech therapy, discharge planning

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62
Q

patent foramen ovale

A

10% of ischemic strokes, allows embolism from venous circulation into arterial circulation to the brain, tx antiplatelet therapy or anticoagulant or surgery

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63
Q

carotid stenosis

A

endarterectomy, greater benefit if greater stenosis, only for pts with >50% stenosis

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64
Q

stroke prevention

A

modifiable risk factors - lower hypertension (140/90), diabetics HA1c <35in waist in women), active 30 min day, antifibrinogen INR 2-3

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65
Q

stroke complications

A

depression, dementia, dysphagia, sexual dysfunction, incontinence, UTI, falls, blood clots, neurologic dysfunction

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66
Q

case - 61, diabetic, HTN, smile droops left, left arm very weak, left leg slightly weak, decreased left side face senation, gaze to the right, can not name things seen on the left - where is stroke???

A

right middle cerebral artery stroke

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67
Q

case - 54, African American, diabetic, HTN, atrial fibrillation - coumadin, high blood sugar, no abnormalities on head CT - next step???

A

lumbar puncture - looking for blood in CNS if there is a hemorrhagic stroke

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68
Q

case - 71, male, HTN management, irregular heart beat with left-side carotid bruit, 40% stenosis of carotid on ultrasound - next Tx???

A

coumadin blood thinner to reduce risk of stroke, greater benefit than aspirin

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69
Q

case - 68, male, episodic unilateral headaches, bumping into things on his right side, all CN and motor exam normal, right visual field deficit - where is stroke???

A

left posterior cerebral artery

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70
Q

case - 63, female, numbness in right arm, unable to speak, symptoms resolved - what test to ID problem???

A

carotid doppler ultrasound - transient ischemic attack was likely in the left middle cerebral artery coming from carotid stenosis

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71
Q

MS and MRI

A

white spots on brain from degradation of myelin creating water which creates H ions (that is what MRIs measure), axial brain with white dots, sagittal brain with white spots, sagittal spinal cord with white spots

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72
Q

MS and evoked potentials

A

apply stimulus in one place and measure action potential in another place, measures nerve conductance, MS shows weaker action potentials and longer latent period

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73
Q

CNS myelin

A

made by oligiodendroctyes processes wrapping axons

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74
Q

PNS myelin

A

schwann cells, entire cells wraps axons

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75
Q

myelin membrane differences from normal CNS cell membranes

A

myelin - 2 lipids : 1 protein (normal cell 1 lipid : 2 protein), more cholesterol, less phopsholipid (ethanolamine dominant instead of lecithin), 4x more galactolipid (cerebrosides, sulfatides), less phosphatidylinostitol that is used in cell signaling pathways

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76
Q

ceramide galactosyltransferase deficient mice (CgT)

A

form myelin with reduced thickness, cytoplasm retention, and disorganized myelin folding

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77
Q

ceramide synthase deficient mice (CerS)

A

form myelin with focal detachments of individual or groups of myelin lamellae

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78
Q

fatty acid 2-hydroxylase (Fa2 h) deficient mice

A

for adding OH group to fatty acid, make normal myelin, but develop myelin degeneration in old age

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79
Q

myelin lipid creation from fatty acids

A

glycerol backbone replaced with ethanolamine backbone and sugar and phosphate attached, also has ether bond (C-O-C) instead of ester bond (O=C)

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80
Q

CNS - proteins in myelin

A

myelin basic protein (MBP), proteolipid protein (PLP), combined = 60-80% of myelin proteins

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81
Q

PNS - proteins in myelin

A

myelin basic protein (MBP), protein 0 (P0), PMP-22 trace protein

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82
Q

myelin sheath structure

A

formed by apposition of external (intraperiodic line) and internal (major dense line) surfaces, cytoplasm squeezed out, MBP holds inner to inner together making dark ring, PLP / P0 with small carb span membrane and hold inner and outer together making light ring

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83
Q

external myelin membrane

A

cholesterol, galactocerbroside, s-galactocerbroside

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84
Q

internal myelin membrane

A

cholesterol, inostoldiphosphate, ethanolamine plasmalogen, P-serine

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85
Q

CNS demyelination diseases

A

myelin degrades, acquired, ex: MS, leukoencephalopathy, encephalomyelitis, central pontine myelolysis, anti-MAG disease

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86
Q

CNS dysmyelinating disease

A

molecular gene defect in myelin, inherited, ex: leukodystrophies, Krabbe disease

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87
Q

PNS acquired neuropathy

A

autoimmune, demyelinating, polyneuropathy, ex: Guillain-Barr Syndrome (acute)

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88
Q

PNS inherited neuropathy

A

dysmyelinating, ex: Charcot-Marie-Tooth disease, Krabbe disease,

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89
Q

Lorenzos Oil

A

movie about leukodystrophy accumulation of long chain fatty acids, Tx with oil with concentrated long chain fatty acids to suppress the synthesis of long chain fatty acids in the body

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90
Q

proteolipidprotein myelin disorders

A

4 transmembrane protein with two external side loops and one internal side loops, holds inner and outer surfaces together, mutations of protein cause disorders, ex: jimpy, rumpshaker, jimpy-msd - most mutations are on external loop

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91
Q

myelin basic protein disorders

A

large protein with 7 exons, if all exons expressed = large protein, if alternative RNA splicing = smaller protein, different sized MBP at different times in life and naturally mixed together, deletion / inversion of part of gene causes disorder

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92
Q

shiverer mutation in myelin basic protein

A

first animal study with effective gene therapy (gene rescue), transfected normal gene improves the amount of myelin

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93
Q

Charcot-Marie-Tooth Disease

A

PNS dysmyelination disease, high arches, claw foot, muscle atrophy in lower legs, make too much myelin, two copies of the proteolipidprotein gene (PMP22) on chromosome

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94
Q

experimental allergic encephalomyelitis

A

animal model for MS, injected with mutated myelin basic protein - animal model for autoimmune CNS demyelinating disorders

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95
Q

experimental allergic neuritis

A

animal model of Guillain-Barre Syndrome, model for autoimmune PNS demyelinating disorders

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96
Q

MS

A

autoimmune, lymphoctyes cross BBB with alpha4beta1 and VCAM1 adhesion molecules, lympocytes release cytokines that call in macrophages, macrophages destroy myelin

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97
Q

MS Tx - natalizumab (Tysabri)

A

molecular antibody against alpha4beta1 lymphocyte adhesion molecules to prevent them from crossing the BBB

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98
Q

demyelinating disorders

A

myeline degradation and sometimes loss of axons, ex: MS, acute disseminated encephalomyelitis (ADEM), acute necrotizing hemorrhagic encephalomyelitis, central pontine myelinosis

99
Q

multiple sclerosis, MS

A

common 1/1000, more F, <50 onset, autoimmune CNS demyelination, relapsing and remitting course of neurologic deficits, white matter lesions, HLA-DR2 antigen presenting cell receptor most likely to get MS, linked to IL-2 and IL-7 receptors, depleted B cells = less likely to get MS, genetic and environmental, optic effects common

100
Q

oligiocolonal bands

A

MS diagnostic, dark gamma area in gel, from various B cell clones making antibodies

101
Q

MS plaques

A

lots, adjacent ventricles or just deep to gray matter, can be in spinal cord too, depressed and firm, active or inactive, white on MRI, dark red in fresh tissue, often follow blood vessels

102
Q

active plaques

A

lipid stuffed macrophages, T cells cuffing vessels, axons present but not myelinated

103
Q

inactive plaques

A

no myelin, decreased oligiodendrocytes, gliosis (astroctytes), decreased axons, empty

104
Q

MS plaques microscopic

A

lighter (no myelin to stain), fewer cells, lymphoctye cuffed vessels, reactive astrocytosis

105
Q

sharply demarcated active plaque around blood vessel

A

two forms - type I with Ig and complement, type II without Ig and complement

106
Q

poorly demarcated active plaque not around blood vessels

A

two types - type III widespread oligodendrocyte apoptosis, type IV central oligodendrocyte apoptosis

107
Q

shadow plaques

A

plaque border indistinct, thin myelin sheaths at edges, possible remyelination?, not an inactive plaque

108
Q

type I and II, type III and VI plaques

A

found with eachother only, suggests more than one mechanism for MS

109
Q

MS central symptoms

A

unilateral visual impairment with optic nerve involvement (often first presentation), cranial nerve signs, ataxia, nystagmus (brainstem involved)

110
Q

MS spinal symptoms

A

motor / sensory impairment in trunk / limbs, spasticity, bladder control problems

111
Q

acute disseminated encephalomyelitis

A

diffuse, monophasic, following viral infection, children, rapid onset, headache, lethargy, coma, fatal 10%, acute autoimmune reaction

112
Q

acute necrotizing hemorrhagic encephalomyelitis

A

very severe and acute, young adults / children, follows upper resp infection, fatal or deficits in survivors, hyperacute variant of acute disseminated encephalomyelitis

113
Q

central pontine myelinolysis

A

symmetric myelin loss in basis pontis and pontine tegmentum, caused by hyponatremia (low Na+) that is corrected too rapidly, rapid quadriplegia / quadraparesis, monophasic, alcoholics, organ transplants, malnutrition

114
Q

human prion disease

A

first documented in 1957 in Fore tribe of Papua New Guinea were tribe practiced cannibalism of the dead, tribe quit eating dead but cases seen for decades due to long latent period

115
Q

Kuru

A

Fore tribe prion disease, strange walk, slurred speech, facial ticks, uncontrolled fits of laughter, death in 6-12 months, more women and children, CBC normal, no cultures, brain autopsy with minimal inflammation, demonstrated human to human transmission with chimp experimentation, incubation of up to 40 years

116
Q

prion (PrPsc)

A

survives boiling, freezing, formaldehyde, carboxylic acid, chloroform, desiccation, UV, nucleases - smaller than a virus - sensitive to proteases, misfolded PrPc protein with more beta sheets, converts (seeds) PrPc to PrPsc creating amyloid

117
Q

amyloids

A

fibrous protein deposit, associated disease, binds congo red and thioflavin T dyes

118
Q

human prion diseases

A

Creutzfeldt-Jakob disease, CJD variant, fatal familial insomnia, kuru

119
Q

animal prion diseases

A

scrapie, mad cow, chronic wasting

120
Q

Creutzfeldt-Jakob disease

A

60s, sporadic, few familial or transmitted, memory / behavior changes, rapid progressive dementia, startle myoclonus, fatal in ~7 months, spongiform brain change but no plaques, no Tx

121
Q

variant Creutzfeldt-Jakob disease

A

young adults, behavior change / depression, slower progression than CJD, more cortical plaques, linked to mad cow disease (spongiform bovine encephalopathy), had eaten infected cow meat, can also be transmitted by blood transfusion, amyloid plaques and spongiform change, no Tx

122
Q

familial fatal insomnia

A

sleep disturbances, ataxia, autonomic problems, coma, inherited mutation of PRNP gene, PrPc similar to CJD, no spongiform change, neuronal loss, death in 3 years, barbituate sleeping pills make worse, no Tx

123
Q

Kuru

A

human prion disease, amyloid plaques and spongiform change, no Tx

124
Q

familial CJD (fCJD)

A

autosomal dominant, no Tx

125
Q

CJD labs

A

EEG - sharp wave complexes, MRI - intense signal in striatum / linear lesions and bilateral posterior thalamus, CSF - high proteins (also encephalitits, cerebral infarct), biochemistry - western blot of PrPsc, DNA sequencing - PRNP gene for fCJD, brain biopsy - spongy change and PrPsc by ELISA and immunochemistry

126
Q

transmissible spongiform encephalopathies

A

cattle to humans causes vCJD, 10 year latent period

127
Q

vCJD

A

20s, 13-14 months, behavior change, painful sensory, delayed neurologic, thalamus MRI sign, plagues, accumulated PrPres, in lymphoid tissue, increased glycoform ratia, genotype of methionine / methionine at codon 129 of PrPc gene

128
Q

classic CJD

A

60s, 4-5 months, dementia, early neurological signs, sharp EEG waves, polymorphic genotype at codon 129 of PrPc gene

129
Q

chronic wasting diseases

A

cervids - deer, elk, moose, middle America into Canada, prion found in urine / feces / saliva / ground water, experimental innoculation of squirrel monkey vs macaques suggests not transmissible to humans, careful butchering and deer tested by DNR

130
Q

human amyloid formation diseases

A

alzheimer, parkinsons, type II diabetes, cataracts - not prion diseases; spongiform encephalitis - prion disease

131
Q

chaperone proteins

A

chaperone proteins establish normal molecular structure and may be a good target to treat human prion diseases

132
Q

Alzheimer compared to CJD

A

slower progression, no muscular effects, no spongiform change (but amyloid plaques like vCJD), tau protein marker (marker fof CJD too)

133
Q

exotoxins

A

secreted from cell, high toxic (1ug fatal), neutralized with high-titer antibodies called antitoxin, heat liable, resistant to digestive enzymes, tx antibiotics / antitoxin / symptomatic

134
Q

toxoid

A

inactive toxin used in vaccine, ex: tetinis shot

135
Q

clostridium tetani

A

gram +, spore forming, rod, anaerobic

136
Q

clostridium tetani

A

spores enter skin via trauma, germinate in anaerobic necrotic tissue, tetanospasmin exotoxin blocks release of glycine and GABA at inhibitory Renshaw cell interneuron causing spastic paralysis / trismus (lockjaw) / respiratory problems, Tx neutralize with human tetanus immune globulins, immunization booster, penicillin, muscle relaxants - can be transmitted by IV drug use

137
Q

clostridium botulinum

A

gram +, spore forming, rod, anaerobic

138
Q

clostridium botulinum

A

spores in water / soil, alkaline canned veggies, exotoxin released on death of cell, infants can get in honey, bilateral cranial nerve palsy with diplopia, dysphagia, muscle weakness, resp problems, floppy baby, flaccid paralysis, prevents release of ACh by blocking vesicle fusion SNARE proteins, Tx antitoxin, immunoglobin, penicillin, ventilator

139
Q

clostridium botulinum (botox) uses

A

muscle spasms, chronic migraine, excessive sweating, crossed eyes, muscular dystrophy

140
Q

corynebacterium diphtheriae

A

gram +, rod, nonmotile, no spores

141
Q

corynebacterium diphtheriae

A

resp droplets to pharynx, possible meningitis, must be lysogenized by bacteriophage to release exotoxin that damages neurons and heart cells by interfering with protein synthesis, peripheral nerve palsies, Guillain Barre-like, palatal paralysis, cranial neuropathy, culture on potassium tellurite agar and Loeffler’s coagulated blood serumn, Tx antitoxin, penicillin, DPT vaccine (exposure does not guarantee immunity)

142
Q

corynebacterium diptheriae mechanism

A

shuts down translation in neurons and heart cells, B subunit binds cell membrane receptor and allow A subunit to enter cell, A subunit inhibits translation by binding elongation factor 2 (EF2)

143
Q

Taenia solium - neurocysticerosis

A

parasitic worm, ingest larvae in uncooked pork, causes neurocysticerosis (swiss cheese brain)

144
Q

Taenia solium - neurocysticerosis life cycle

A

pigs and human, scolex head allows attachment in intestine and eggs / proglottids in feces, cysterol in muscles / subcu / brain / eyes

145
Q

heamatogenous spread to CNS

A

H. influ, N. meningitidis, Strep p, mycob tuberculosis, fungi, enteroviruses

146
Q

other routes of spread to CNS

A

trauma, surgery, intraneural

147
Q

intra-neural spread to CNS

A

rabies - along sensory nerves, herpes along trigeminal or sacral nerves, poliovirus, togavirus

148
Q

infections that can be transferred from mother to child with CNS involvement

A

herpes (HS2), H. influ, chlamydia, strep B, CMV, N. gonorrhea (conjunctivitis), HIV, E. coli, toxoplasmosis

149
Q

CNS disease that transfer from mother to fetus

A

group B strep, listeria monocytogenes, E. coli - causing acute bacterial sepsis or meningitis; N. gonorrhoeae - conjunctivitis; Chlamydia trachomatis - conjunctivitis; congenital syphillis - neurosyphillis

150
Q

Treponema pallidum

A

neurosyphilis, subacute meningitis, Argyll - Robertson pupil (does not react to light, does react to convergence), meningovascular syphilis, tabes dorsalis, paresis

151
Q

tabes dorsalis

A

untreated traponema pallidum, syphillis, damage to posterior column and dorsal roots, ataxia, loss of reflexes, loss of pain and temp sensation

152
Q

general paresis

A

untreated treponema pallidum, syphillis, mental deterioration, psychiatric symptoms

153
Q

congenital syphillus

A

untreated treponema pallidum, crosses placenta, high mortality, CN VIII deafness

154
Q

infections that can cross placenta (TORCHES)

A

T - toxoplasmosis, O - other (HIV), R - rubella / chorioretinitis, C - cytomegalovirus, H - herpes simplex

155
Q

herpes labialis - HSV1

A

keratoconjunctivitis - dendritic ulcers, temporal lobe encephalitis, via trigeminal ganglia, Tx acyclovir and topical trifluridine

156
Q

herpes genitalis - HSV2

A

aseptic meningitis, myelitis, neonatal meningitis, cervical carcinogenesis, via sacral ganglia, Tx acyclovir

157
Q

varicella zoster virus - chicken pox, shingles

A

meningoencephalitis, keratitis, via trigeminal nerve or dorsal root ganglia, Tx acyclovir and varicella vaccine

158
Q

ebstein bar virus - infectious mononucleosis

A

meningoencephalotiti, via B lymphocytes, Tx self limiting

159
Q

cycolomegalovirus

A

encephalitis, chorioretinitis, Alzheimer, via mononuclear cells, Tx ganciclovir

160
Q

cerebral palsy

A

is a type of static encephalopathy, traumatic brain injury involving blood flow and O2, perinatal, may not show right away after birth, milder will take longer to show up, premature babies may have for no apparent reason, shows by 2 years

161
Q

premature cerebral palsy

A

blood vessel aren’t pruned yet, periventricular injury, frontal lobe fibers to legs affected (spastic biplegia), arms fine

162
Q

term cerebral palsy

A

injury where cerebral arteries are after blood vessels have been pruned, arms will be more affected than legs

163
Q

autism

A

improves for most, personality profile, primary - seen alone, syndrome - seen with other problems, spectrum disorder, other delays common

164
Q

neurologic syndromes

A

if diagnosed are useful, give family genetic counseling and prognosis infromation

165
Q

leukodystrophy

A

don’t want to miss, white matter injury that is diffuse, progresses, gets worse, loss of motor ability, autosomal recessive, tx bone marrow transplant, looks like cerebral palsy but later onset, ex: child learns to walk and then loses ability to walk

166
Q

congenital stroke

A

may not show until 6-12 months due to dominant extra pyramidal system that is bilateral

167
Q

muscular dystrophy

A

normal until 2-4 years old, gradual decline

168
Q

epilepsy

A

many causes, infantile spasms, don’t want to miss, can be generalized, focal, secondarily generalized, EEG determines Tx, should have loss of consciousness

169
Q

generalized epilepsy

A

spike in one area of EEG

170
Q

focal epilepsy

A

spikes on many parts of EEG

171
Q

benign epilepsy disorder

A

seizures on face, normal EEG, outgrow most of the time

172
Q

non-epileptic seizures

A

look like seizures but are not, no loss of consciousness, many with psychological causes, ex: syncope (fainting), panic, hypertventilation, gastroesphageal reflux / Sandifer’s syndrome, tic disorders (can control)

173
Q

Sandifer’s syndrome

A

gastroesophageal reflux, stiffness, turn blue, hold breath, not a seizure

174
Q

impulse control disorders

A

ADHD, OCD, Tourette, tic - can be seen in same pt or in same family

175
Q

static encephalopathy

A

single incident of injury to the brain, does not progress, ex: infection or cerebral palsy

176
Q

central pontine myelinolysis

A

acute demyelination in basilar pons, interrupts corticobulbar and corticospinal tracts, preserves sensory input, rapid quadriplegia, too rapid correction of hyponatremia (should be 1 mEq/L/hr)

177
Q

diabetic neuropathy / vit B12 deficiency

A

decreased ankle reflexes and leg sensation

178
Q

ataxic gate

A

alcohol intoxication or cerebellar vermis atrophy

179
Q

multiple sclerosis

A

demyelination in CNS, symptoms separated in time and space in white matter, episodes last longer than 24 hours, autoimmune attack of oligodendrocytes, periventricular plaques on MRI, optic neuritis in one eye common

180
Q

bilateral lesion of pyramidal tract at pyramidal decussation

A

fine hand control deficits, loss of thumb / index finger opposition and digit extension leads to cupping of hand, reaching / locomotion / larger movement intact, shows in finer motor control because there are other intact systems contributing to gross motor control

181
Q

upper motor neuron syndrome

A

lesion of primary motor cortex, all contralateral effects that include weakness in one side (paresis), increased extensor tone, increased stretch reflex, positive Babinski sign, fine motor deficits (hand/foot/mouth/tongue), corticobulbar signs of affected cranial nerve nuclei

182
Q

corticobulbar signs of primary motor cortex lesion - lower quadrant facial muscles

A

contralateral side, lateral part of CN VII nuclei, loss of smiling, baring of teeth, and puffing of cheeks - can put eyerbrows up and wrinkle forehead because that is ipsilateral and contralateral CN VII innervation

183
Q

corticobulbar signs of primary motor cortex - accessory nucleus lesion

A

weakness of ipsilateral trapezius and sternocleidomastoid (turns head toward opposite side of body)

184
Q

corticobulbar signs of primary motor cortex - hypoglossal nucleus lesion

A

weakness of contralateral tongue, tongue protrudes toward weak side

185
Q

stroke in primary motor cortex

A

paresis, recovered proximal joint function, no extension of digits, buttoning and using fork hard, clumsy fingers, didn’t know next move, mental effort to do things

186
Q

lesion of premotor cortex

A

can’t execute complex motor plans that require visuomotor transformation (ex: reaching around a clear barrier to grasp food), can’t steer arm correctly, can’t learn new sensory-motor associations (ex: stopping at a stop sign when driving)

187
Q

lesion of supplementary motor area

A

deficits in internally driven and sequenced movements, pt is stimulus bound and will react to a sensory stimulus no matter where they are (ex: urinal in public place), alien hand syndrome (sense that someone else is moving their hand), trouble with learned sequences leading to semi-purposeful movements outside pt control

188
Q

vestibulocerebellum disorder

A

equilibrium/balance disturbed (fall toward side of lesion), nystagmus, loss of smooth pursuit (can’t follow moving object smoothly, follow with saccadic eye movement), wide based gate to add stability — drunk, cerebellum is sensitive to alcohol

189
Q

lesion of fastigial nucleus

A

affects vestibulocerebellum, loss of equilibrium/balance, nystagmus, loss of smooth eye pursuit (replaced by saccadic), wide based gate

190
Q

lesion of spinocerebellum

A

disorders ipsilateral to side of lesions, ataxic gate if vermis involved, hypotonia (not weak), action/target/intention tremor, limb dysmetria, timing off, movement decomposition into individual joint movements

191
Q

lesions of emboliform and globose nuclei

A

disorders ipsilateral to side of lesions, ataxic gate if vermis involved, hypotonia (not weak), action/target/intention tremor, limb dysmetria, timing off, movement decomposition into individual joint movements

192
Q

cerebrocerebellum lesions

A

interacts with contralateral side of cortex, effects ipsilateral side of body, ataxia of finest movements (hand shape, writing), possible cognitive effects

193
Q

lesion of dentate nucleus

A

interacts with contralateral side of cortex, effects ipsilateral side of body, ataxia of finest movements (hand shape, writing), possible cognitive effects

194
Q

hypotonia

A

= cerebellar problem, not weakness, ex: limb can flex completely without resistance but with arm held up hand will drop

195
Q

hypertonia

A

not cerebellum, some other problem, likely lack of inhibtion to thalamus

196
Q

case - left side paresis / paralysis in leg

A

likely a stroke in the right anterior cerebral artery, causes left sided paresis / paralysis and leg part of motor homunculus is in the interhemispheric fissure which is suppied by the anterior cerebral artery

197
Q

upper motor neuron lesion

A

CNS, hyperreflexia, weakness, paralysis, hypertonia, spasticity, no abdominal reflex, positive Babinski, muscle fasciculations

198
Q

lower motor neuron lesion

A

spinal/peripheral, hyporeflexia, muscle atrophy, hypotonia, weakness, paralysis, normal abdominal and plantar (negative Babinski) reflexes

199
Q

lesion of subthalamic nucleus

A

commonly stroke, hyperkinetic dyskinesia, ballismus (wild exaggerated limb movement on contralateral side), due to loss of subthalamic excitation of globus pallidus internus which inhibits thalamus

200
Q

Parkinson

A

loss of cells in substantia nigra compacta in dopamine loop leading to decreased dopamine levels, direct pathway no longer inhibits globus pallidus internus and indirect pathway stimulates globus pallidus internus to inhibit thalamus, decreased thalamic activity = decreased movement

201
Q

Parkinson clinical findings

A

bradykinesia / akinesia, rigidity, resting tremor from over inhibited oscillating signal of thalamus, postural instability

202
Q

causes of parkinson

A

possible oxidative stress, encephalitis lethargica (viral encephalitis epidemic after WWI - destroyed substantia nigra compacta), toxins (CO, Mn), head trauma (bowers)

203
Q

Parkinson Tx

A

restore dopamine levels with L-DOPA, can produce hyperkinetic movements (shakes)

204
Q

globus pallidus lesion

A

removes tonic globus pallidus internus inhibition of thalamus, flexion dystonia/posturing, dytonia/rigidity from increased motor activity

205
Q

putamen lesion

A

motoric, hyperactive, stereotypic, part of movement repeated

206
Q

caudate lesion

A

complex changes, cognitive disorders with hyperactivity, vulgarity, implusiveness, increased appetite, polydipsia, hypersexuality

207
Q

huntington chorea (dance)

A

autosomal dominant, short arm on chromosome 4, CGA gain of function repeat, 25-40 yr onset, death of GABA/ENK spiny neurons in neostriatum, loss of cerebral cortex neurons, striatum dies, effects indirect pathway - allows GPe to inhibit STh from stimulating GPi which would inhibit thalamus, thalamus increases activity, involuntary chorea or athetosis, dementia, cognitive decline, akinesia

208
Q

involuntary movements

A

indirect pathway is affected, GPi is not inhibiting thalamus

209
Q

akinesia

A

direct pathway effected, GPi no longer inhibited allow for tonic activation of thalamus

210
Q

case - 26, white male, involuntary movement of limbs, body, trunk, progressive, loss of cognitive function, father had disease

A

huntington

211
Q

case - 30, white male, MVA, head injuries, comatose, increased extensor tone in arms / legs

A

decerebrate rigidity, emergency, must relieve pressure on brain

212
Q

huntington pathogenesis

A

loss of basal ganglia neurons (especially spiny striatal neurons) leads to increased motor output, neuron loss in cortex leads to cognitive changes

213
Q

gross features of huntington

A

small brain, atrophy of striatum (especially caudate), atrophy of frontal lobe, dilated lateral / 3rd ventricles due to fill space left by atrophy (hyrdocephalus ex vacuo)

214
Q

microscopic features of huntington

A

neuronal loss and astrocytosis (gliosis), ubiquitin tagged Htt protein forms aggregates (should be eaten by proteasome), aggregates contain protein with 40+ glutamines that make thin, threadlike aggregates

215
Q

lacunar infarct

A

involves penetrating branches of middle cerebral artery called lateral striate arteries, supply caudate, putamen, globus pallidus, and internal capsule, causes small cavitary lesions around arteries in lateral striate, common with long standing hypertension, common in basal ganglia and thalamus

216
Q

lesion of primary motor cortex in interhemispheric fissure on both sides

A

paraplegia, paralysis of both legs

217
Q

Urbach-Wiethe disease

A

bilateral calcification of amygdala, trouble recognizing fear in facial expression, trouble distinguishing between similar emotions, memory loss of emotional content (need amygdala to pair neutral stimulus and harmful stimulus)

218
Q

post traumatic stress disorder

A

re-experience, avoidance, hyperarousal, prefrontal cortex activity decreased, amygdala activity increased, prefrontal cortex normally inhibits anygdala

219
Q

schizophrenia

A

fragmentation of mood / motivation / movement, positive delusions / hallucination, negative social withdrawal / loss of executive function, Tx on effect positive symptoms, 1% pop, dopamine and glutamate hypotheses of causation

220
Q

dopamine hypothesis - schizophrenia

A

increased DA receptor activity, ex: amphetamines cause schizophrenic-like symptoms by increasing DA release and blocking DA reuptake, target for typical and atypical anti-psychotics

221
Q

glutamate hypothesis - schizophrenia

A

phencyclidine (PCP) causes schizophrenia like symptoms by blocking NMDA glutamate receptors, possible tx by increasing glutamate

222
Q

depression

A

fatique, anhadonia, social withdrawal, 20% women, 13% men, ~17% pop, monoamine hypothesis - decreased norepinephrine / serotonin activity, tx monoamine oxidase inhibitors, tricyclics, specific serotonin reuptake inhibitors

223
Q

Korsakoff’s syndrome

A

no new memories, disoriented in space and time, confabulation in response to questions, chronic alcoholism with thiamine (vit B1) deficiency, affects mammillary bodies and mamo-thalamic tract

224
Q

Kluver-Bucy syndrome

A

bilateral medial temporal lobe damage, same damage from herpes encephalitis, oral tendencies, loss of emotion (neutral affect) due to amygdala dysfunction, hypersexuality due to hypothalamus dysfunction, visual agnosia (loss of visual cortex input)

225
Q

Alzheimer

A

progressive, loss of memory, mood disorder (anxiety/depression), motor dysfunction, loss of cognitive function, 50% of pop > 80, loss of cholinergic input from nucleus basalis to hippocampus, loss of neurons, neurofibrillary tangles (phosphorylated tau proteins) and beta-amyloid plaques, huge sulci / ventricles due to brain matter loss, tx donepezil (aricept)

226
Q

chronic traumatic encephalopathy

A

neurodegenerative, repeated head trauma, loss of memory / executive function, depression / apathy, impulsiveness / aggressiveness, 30-50, APO e4 allele increases, contact sports, atrophy of frontal / temporal lobes, neurofibrillary tangles with phosphorylated tau proteins in hippocampus and amygdala

227
Q

Weber syndrome

A

superior alternating hemiplegia, ipsilateral oculomotor nerve dysfunction on one side of face and motor dysfunction on contralateral side of body

228
Q

medial pontine syndrome

A

middle alternating hemiplegia, ipsilateral abducens dysfunction (LR), motor and touch sensation dysfunction on contralateral side of body

229
Q

lateral pontine syndrome

A

CN VII / VIII dysfunction, loss of pain and temp sensation on contralateral body, loss of trunk and limb muscle control on contralateral side of body, loss of face pain and temp sensation on ipsilateral side of body

230
Q

medial medullary syndrome (inferior)

A

hypoglossal alternating hemiplegia, hypoglossal dysfunction on ipsilateral side (tongue deviates toward bad side), loss of motor on contralateral side of body, loss of touch sensation on contralateral side of body

231
Q

Wallenberg syndrome (PICA syndrome)

A

lateral medullary syndrome (superior), CN IX and CN X dysfunction on ipsilateral face, loss of pain and temp on contralateral body, loss of trunk and limb coordination on contralateral body, loss of pain and temp sensation on ipsilateral face

232
Q

Parkinson

A

60, unilateral resting tremor, small hand writing, worse when anxious, anosmia, monotone voice, masked face, slowed rapid hand movements, arm does not move when walking, hard to initiate walk, shuffle bent forward walk

233
Q

Mn toxicity parkinsonism

A

all symptoms similar to parkinson but does not respond to tx as well - common with welders, more general symptoms, heavy metals do not go away

234
Q

parkinson pathology report

A

decreased pigmentation in substantia nigra and locus ceruleus, decreased neurons in substantia nigra, Lewy bodies

235
Q

deep brain stimulation

A

used on globus palludis internus in parkinson to reduce inhibition of thamalus

236
Q

diabetes insipidus

A

trauma / pituitary stalk section/autoimmune/idiopathic, increased urination (polyuria), increased thirst (polydipsia), due to lack of vasopressin from posterior pituitary, tx desaminovasopressin only acts on kidneys - not smooth muscle

237
Q

galactorrhea-amenorrhea

A

hyperprolactinemia and amenorrhea (lactation and no period), prolactin level high, lutenizing and follicle stimulating hormones low, pituitary microadenoma, tx surgery or dopamine to inhibit prolactin secretion

238
Q

Prader-Willi syndrome

A

deletion of chrom 15, fetal hypotonia, mild mental retardation, hypogonadotropic hypogonadism (low LH, low FSH, low gonadal function), obesity due to hyperplegia from excessive ghrelin secretion

239
Q

basilar stroke

A

rostral brainstem and occipital lobe affected, CN palsy - gaze problems, hemianopsoa, miosis, damage to reticular activating system causes altered / loss of consciousness; only type of stroke with loss of consciousness

240
Q

loss of consiousness seizures

A

must be reported to the DMV or dept of public safety

241
Q

MS

A

can be minicked in animals by injecting bacterial toxins

242
Q

Mn poisoning

A

can cause hallucinations

243
Q

destruction of substantia nigra compacta

A

decreases firing in ventral lateral thalamus

Week 4 - Neuro (5 decks)

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