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HD 2 > Neurology > Flashcards

Neurology Flashcards

0
Q

crossed hemisyndrome

A

when one side of the face has a neurological deficit, and the opposite side of the body also has (the same?) deficits;
= due to a brainstem lesion!

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1
Q

Hemiparesis

A

loss of motor control due to a cortical or subcortical hemispheric lesion

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2
Q

myopathy

A

muscle weakness with preserved sensation & reflexes

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3
Q

pseudoathetosis

A 
(athetosis = unintentional writhing of hand;) 
pseudoathetosis = subconscious hand writhing due to loss of proprioception.
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4
Q

Stroke

A

sudden, focal brain dysfunction;

Caused by cerebral ischemic or hemorrhagic events.

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5
Q

Lewy Body

A

abnormal protein accumulation common in Parkinson’s Disease.

  • circular, dark intracellularl;
  • contains alpha-synuclein, ubiquitin, and other proteins
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6
Q

Cardinal signs of parkinsonism

A

“TRAP”

  1. Tremor
  2. Rigidity
  3. Akinesia/bradykinesia
  4. Postural changes
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7
Q

Causes of parkinsonism

A

1. Parkinson’s Diseases (idiopathic or genetic)

  1. Atypicals: Multiple System Atrophy (MSA), Lewy Body Disease, Progressive Supranuclear Palsy (PSP), corticobasal degeneration.
  2. drugs, toxins (antipsychotics, MPTP, CO)
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8
Q

path signs of frontotemporal dementia

A

Tau-like deposits & Pick bodies in fronto-temporal lobes;

Macro: cerebral atrophy

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9
Q

path signs of Lewy Body Dementia

A

location: fronto-temporal lobe
Macro: cerebral atrophy
Micro: Lewy Bodies

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10
Q

path signs of Huntington’s disease

A

Location: basal ganglia
Macro: neostriatal atrophy
Micro: neuron loss & astrocytosis
** chorea! **

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11
Q

path signs of ALS (Amylotrophic Lateral Sclerosis)

A

Location: motor cortex, brainstem and spinal cord (anterior horn)
Macro: motor neuron and muscle atrophy
Micro: inclusion bodies (look similar to Lewy bodies, but in spinal cord)

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12
Q

Path signs of Parkinson’s disease

A

Location: midbrain (substancia nigra & locus ceruleus)
Macro: loss of pigmentation in substancia nigra (was blue - dopamine)
Micro: Lewy Bodies w/ a-synuclein
** akinesia/bradykinesia + resting tremor **

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13
Q

Path signs of Alzheimer’s Disease

A

Location: temporo-parietal; ApoE or Presenilin mutations.
Macro: cerebral atrophy
Micro: neurofibrillary tangles (tau), b-amyloid plaques
** memory loss, decreased self-care/f(x) **

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14
Q

Prion disease

A

Location: diffusely through cortex
Macro: cerebral atrophy
Micro: prion protein deposits, neuron loss & reactive gliosis
Sx: progressive dementia + myoclonus

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15
Q

steps in assessment after 1st grand mal seizure

A
  1. take history (ask about drug use!)
  2. EEG: look for spikes (focal or generalized)
  3. imaging - CT or MRI: to ID structural abnormalities or other pathology (tumors, hemorrhage, etc)
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16
Q

Subarachnoid hemorrhage

A

“Worst headache of life,” often from rupture of cerebral hemorrhage

  • can cause stroke
  • risk secondary infarction due to P.Com. artery spasm up to 1 wk after initial hemorrhage.
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17
Q

Top causes of intracranial hemorrhage (–> stroke)

A

1 HTN -> microvascular rupture (esp. brainstem?)

  1. Amyloid angiopathy (esp. cortex, >80 yrs old)
  2. Vascular malformation
  3. Bleeding metastatic lesion
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18
Q

4 steps in pain processing

A
  1. Transduction: convert stimulus to action potential
  2. Transmission: send AP to brain
  3. Modulation: esp. by 5-HT & NE at dorsal horn (inhibitory), *targeted by pain meds!
  4. Perception: subjective, influenced by cultural factors and biological sensitization
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19
Q

Pain pathway (from mechanical stimulus to neural processing)

A

NocioR –> peripheral n. -> DRG (dorsal root ganglion) -> spinal cord -> thalamus -> brain (somatosensory cortex, frontal cortex & limbic system)

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20
Q

Clinical signs of Late Parkinson’s disease

A

decreased facial expression, decreased arm swing w/ walk, shuffling walk, decreased vocal volume

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21
Q

Progressive Supranuclear Palsy (“PSP”) clinical signs

A

(atypical parkinsonism)

  • limited upward & downward gaze
    • -> furrowed brow and startled expression;
  • axial rigidity –> early falls (esp. backwards)
  • hummingbird sign on MRI
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22
Q

Multiple System Atrophy (“MSA”) clinical signs

A

(atypical parkinsonism)

  • early ANS & cerebellar dysfunction –> ataxia
  • does NOT respond well to levodopa
  • cerebellar & basal ganglia atrophy on MRI
23
Q

Corticobasal Syndrome/Degeneration (“CBS/CBD”) clinical signs

A

(atypical parkinsonism)

alien limb and symmetric apraxia

24
Q

Wilson’s Disease clinical signs

A

(atypical parkinsonism)

  • movement disorders/ataxia
  • psych disorders
  • liver disease!
  • low copper levels in blood & Kayser-Fleischer ring in iris
25
Q

Lewy Body Disease (“LBD”) clinical signs

A

(atypical parkinsonism)

  • cognitive fluctuations
  • hallucinations
  • falls
  • w/ diffuse a-synuclein mutations
26
Q

Acute subdural hematoma

A

cortical laceration and vascular injury (of cortical aa or bridging vv), progressively decreasing consciousness and increasing neuro Sxs.
-> concave hypERdensity on CT (on brain surface)
Tx: intubate, hyperventilate, mannitol, & craniotomy
50% mortality!

27
Q

Chronic subdural hematoma

A

mild headache w/ progressive personality changes/dementia;
*in elderly, may not have specific Hx of trauma (esp. if + anticoag.)
–> concave hypOdensity on brain surface w/ CT, no skull fracture
Tx: Burr hole evacuation +/- catheter, anticonvulsants if Hx of seizure
*usually resolve well.

28
Q

intracerebral hematoma

A

focal neuro Sxs w/ Hx of severe (penetrating) trauma, maintain consciousness.
–> hypERdensity IN brain parenchyma on CT
Tx: NO surgery unless very severe.

29
Q

Acute epidural hematoma

A

Headache, nausea, & decreasing consciousness – usually after a “lucid period” (2-48 hrs), esp. in younger ppl.
usually laceration of Middle Meningeal a. w/ skull fracture (but no parenchymal trauma)
–> Lentiform hypERdensity on CT
Tx: intubate, hyperventilate, mannitol, & craniotomy

30
Q

Appropriate treatment for peripheral nerve injury

A

a) sharp laceration: surgical repair ASAP
b) gunshot wound: surgical exploration & mark, but wait to repair
c) non-penetrating: monitor for 3 months (surgery only if need later)

31
Q

Causes of insomnia

A

(canNOT sleep)

  • Psychophysiological: acquired hypervigilant state
  • Restless Leg Syndrome
  • Circadian Rhythm Delay: inadequate timing or volume of sleep (esp. shift workers)
32
Q

4 main symptoms of restless leg syndrome

A
  1. Leg discomfort (“creepy crawly” sensation)
  2. compulsion to move
  3. movement relieves discomfort
  4. worse at night and interferes w/ sleep
33
Q

major features of Narcolepsy

A

excessive daytime sleepiness and CATAPLEXY (bulbar weakness elicited by strong emotions)
+/- auditory hallucinations just before sleep or just after wake up.

34
Q

Pathophysiology of Narcolepsy

A

= autoimmune destruction of orexin neurons,

so less orexin in Reticular Activating System (lateral hypothalamus).

35
Q

Multiple Sclerosis pathophysiology

A

Autoimmune process:
Autoreactive T cells attack CNS –> B cells take residence in CNS –> make oligoclonal IgG specifically in the CNS (distinct from serum IgG)
=> perivascular inflammation and demyelination -> axon loss acutely, glial scar/plaque chronically.

36
Q

Multiple Sclerosis clinical picture

A

Sx: acute attacks of neuro Sxs, w/ progressive permanent deficits
ie: monocular vision loss, focal numbness & motor deficits, brainstem problems (diplopia, vertigo, hearing loss, facial weakness), impaired gait & impaired bowel/bladder function.
Dx: T2 MRI & CSF (w/ CNS IgG oligoclonal bands)
Tx: corticosteroids acutely, disease-modifiers to prevent relapse
**most often F, ~age 30.

37
Q

Types of Multiple Sclerosis

A
  1. Relapsing-Remitting (RRMS): return to 100% normal in remission
  2. Secondary Progressive (SPMS): some residual deficits, progression from RRMS
  3. Primary Progressive (PPMS): worsens, no remission, M=F!
  4. Progressive Relapsing (PRMS): rare.
38
Q

1st line Disease modifying treatments for Multiple Sclerosis

A

1. interferon B (IFN-B): IV, antiviral & immune-modulatory

*SE: hepatotoxic, spasticity, depression or Glatiramer acetate: block Ag presentation, shift T cells
*SE: lipotropy
39
Q

2nd line disease modifying therapy for Multiple Sclerosis

A

(immunosuppressants, risk other illness)
- Natalizumab: monoclonal Ab to a4-integrin (lymphocyte adhesion)
*SE: PML, hepatoxic
- Mitoxantrone: disrupts DNA synth/repair. for SP or RRMS
*SE: heart failure (cardiotoxic), leukemia
- Fingolimod: oral, block lymphocyte migration
(also Teriflunomide and Dimethyl fumarate)

40
Q

Neuromyelitis Optica (NMO)

A

inflammatory CNS attack by anti-AQP4 autoAb, F>M
–> optic neuritis & transverse myelitis (of spinal cord)
Dx: Long spinal cord lesion (>3 vertebrae), NMOIgG, MRI to rule out MS
Tx: Methylprednisone, plasma exchange; or immunosuppression.
1st line MS drugs NOT effective

41
Q

Acute Disseminated Encephalomyelitis (ADEM)

A

*mostly in children, = post-infectious/post-vaccine (rare now).
Sx: prodrome w/ fever, nausea, headache; onset w/ rapidly progressing stiff neck, multi-focal neuro Sxs, altered mental status!
Dx: WBC > 50, no oligoclonal bands
Tx: steroids (tapered) to prevent relapse. Usually full recovery

42
Q

Path signs of MSA (Multiple System Atrophy)

A

oligodendroglial inclusion bodies reactive to a-synuclein & ubiquitin,
ANS symptoms & does not respond to L-DOPA

43
Q

Path signs of PSP (Progressive Supranuclear Palsy)

A

tau-reactive glial & neuronal tangles w/ silver stain,
in subcortical sites (substancia nigra, GP, midbrain)
loss of voluntary vertical gaze

44
Q

path signs of Cortico-Basal Degeneration (CBD)

A

Gross: cortical atrophy
Micro: Tau inclusions + ballooned neurons
in cerebral cortex (near sulcus), caudate, putamen, & substancia nigra
aphasia = major Sx

45
Q

Friedrich’s Ataxia

A

Aut Recessive (frataxin mut.), young onset;
Sx: gait ataxia hyporeflexia, + cardiomyopathy/myocarditis
Path: deep cerebellum & spinal cord degeneration
* w/ spared cerebellar cortex

46
Q

Spinal muscular atrophies

A

loss of lower motor neurons only.
* NO proximal neuronal tract degeneration
= Aut Dominant, SMN-1 mut.
- infantile (Werdnig-hoffman), intermed., late (Kennedy’s disease)

47
Q

Spina bifida occulta vs. cystica

A

Occulta: asymptomatic bc no spinal cord herniation; spinal process absence.
Cystica: herniated spinal tissue = meningocele (just meninges) or myelomeningocele (spinal cord)

48
Q

Arnold-Chiari Malformation

A
  1. Myelomeningocele (spina bifida cystica) - neuro deficits
  2. Vermis herniation (from shallow posterior fossa)
  3. Aqueduct stenosis –> hydrocephalus
  4. downward displaced pons
49
Q

dysraphism

A

= failure of neural tube closure.

ie: spina bifida, encephalocele, anencephaly, holoprosencephaly

50
Q

Neuro-Glial migration abnormalities

A
  • associated w/ seizures bc thicker cortex/abnormal tissue structure
  • Lissencephaly (smooth brain)
  • Polymicrogyria (small gyri @ temporo-parietal)
  • neuronal heterotopia (neurons in white matter bc incomplete migration)
51
Q

Neurofibromatosis type 1 vs. type 2

A

NF-1: chrom. 17 mut, periph. -> skin lesions (vonRecklinghausen)

NF-2: chrom. 22 mut, Central –> bilat. acoustic schwannoma!, meningiomas/gliomas, lens opacity, cerebral calcification

52
Q

1 insult to pre-term infant brain

A

Subependymal/Intraventricular Hemorrhage.
= hemorrhage bc can’t autoregulate cerebral BP
(hyaline membrane disease & Resp. distress –> rapid BP changes –> blood flow surges in brain => hemorrhage & herniation)

53
Q

ischemic injury in infants

A

mostly white matter lesions esp. if premature.
1. Periventricular leukomalacia - premature
2. Multicystic encephalomalacia - full term, honeycomb cavities
…etc.

54
Q

most common perinatal CNS infections

A
  1. CMV infection (hydrocephalus, CMV inclusion bodies)
  2. toxoplasmosis -> necrotizing meningoencephalitis if severe!
    (hydrocephalus, ocular inflamm, megaencephaly)
  3. HIV
56
Q

path for Acute Disseminated Encephalomyelitis (ADEM)

A 
#1: Perivenular lymphocyte infiltration of CNS, & demyelination by macrophages
- extensive inflamm. infiltrates throughout brain parenchyma
59
Q

Multiple Sclerosis pathology

A

inflammatory CNS demyelination, w/ acutely intact axons (some degradation w/ chronic bc ion channels moved)
Gross: discolored plaques @ optic n & near ventricles
Histo: astrocytosis & macrophage infiltration

HD 2 (14 decks)

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