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Neurology Flashcards

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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

Study These Flashcards
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

Study These Flashcards
A

(atypical parkinsonism)

alien limb and symmetric apraxia

24
Wilson's Disease clinical signs
(atypical parkinsonism) - movement disorders/ataxia - psych disorders - liver disease! * low copper levels in blood & Kayser-Fleischer ring in iris
25
Lewy Body Disease ("LBD") clinical signs
(atypical parkinsonism) - cognitive fluctuations - hallucinations - falls * w/ diffuse a-synuclein mutations
26
Acute subdural hematoma
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
Chronic subdural hematoma
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
intracerebral hematoma
focal neuro Sxs w/ Hx of severe (penetrating) trauma, maintain consciousness. --> hypERdensity IN brain parenchyma on CT Tx: NO surgery unless very severe.
29
Acute epidural hematoma
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
Appropriate treatment for peripheral nerve injury
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
Causes of insomnia
(canNOT sleep) - Psychophysiological: acquired hypervigilant state - Restless Leg Syndrome - Circadian Rhythm Delay: inadequate timing or volume of sleep (esp. shift workers)
32
4 main symptoms of restless leg syndrome
1. Leg discomfort ("creepy crawly" sensation) 2. compulsion to move 3. movement relieves discomfort 4. worse at night and interferes w/ sleep
33
major features of Narcolepsy
excessive daytime sleepiness and CATAPLEXY (bulbar weakness elicited by strong emotions) +/- auditory hallucinations just before sleep or just after wake up.
34
Pathophysiology of Narcolepsy
= autoimmune destruction of orexin neurons, | so less orexin in Reticular Activating System (lateral hypothalamus).
35
Multiple Sclerosis pathophysiology
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
Multiple Sclerosis clinical picture
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
Types of Multiple Sclerosis
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
1st line Disease modifying treatments for Multiple Sclerosis
#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
2nd line disease modifying therapy for Multiple Sclerosis
(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
Neuromyelitis Optica (NMO)
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
Acute Disseminated Encephalomyelitis (ADEM)
*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
Path signs of MSA (Multiple System Atrophy)
oligodendroglial inclusion bodies reactive to a-synuclein & ubiquitin, *ANS symptoms & does not respond to L-DOPA*
43
Path signs of PSP (Progressive Supranuclear Palsy)
tau-reactive glial & neuronal tangles w/ silver stain, in subcortical sites (substancia nigra, GP, midbrain) *loss of voluntary vertical gaze*
44
path signs of Cortico-Basal Degeneration (CBD)
Gross: cortical atrophy Micro: Tau inclusions + ballooned neurons in cerebral cortex (near sulcus), caudate, putamen, & substancia nigra *aphasia = major Sx*
45
Friedrich's Ataxia
Aut Recessive (frataxin mut.), young onset; Sx: gait ataxia hyporeflexia, + cardiomyopathy/myocarditis Path: deep cerebellum & spinal cord degeneration * w/ spared cerebellar cortex
46
Spinal muscular atrophies
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
Spina bifida occulta vs. cystica
Occulta: asymptomatic bc no spinal cord herniation; spinal process absence. Cystica: herniated spinal tissue = meningocele (just meninges) or myelomeningocele (spinal cord)
48
Arnold-Chiari Malformation
1. Myelomeningocele (spina bifida cystica) - neuro deficits 2. Vermis herniation (from shallow posterior fossa) 3. Aqueduct stenosis --> hydrocephalus 4. downward displaced pons
49
dysraphism
= failure of neural tube closure. | ie: spina bifida, encephalocele, anencephaly, holoprosencephaly
50
Neuro-Glial migration abnormalities
* 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
Neurofibromatosis type 1 vs. type 2
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
#1 insult to pre-term infant brain
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
ischemic injury in infants
mostly white matter lesions esp. if premature. 1. Periventricular leukomalacia - premature 2. Multicystic encephalomalacia - full term, honeycomb cavities ...etc.
54
most common perinatal CNS infections
1. CMV infection (hydrocephalus, CMV inclusion bodies) 2. toxoplasmosis -> necrotizing meningoencephalitis if severe! (hydrocephalus, ocular inflamm, megaencephaly) 3. HIV
56
path for Acute Disseminated Encephalomyelitis (ADEM)
``` #1: Perivenular lymphocyte infiltration of CNS, & demyelination by macrophages - extensive inflamm. infiltrates throughout brain parenchyma ```
59
Multiple Sclerosis pathology
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

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