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Neuro 2 > Brain stuff > Flashcards

Brain stuff Flashcards

1
Q

ALS

A

Rapidly progressive, fatal neurodegenerative disease that attacks the neurons responsible for controlling voluntary muscles
This has UMN and LMN lesions

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2
Q

how does ALS present

A

Presents with spasms and weakness which is from the UMN and LMN, very uncommon for neuro problems.
In 3 areas is definite ALS

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3
Q

S of UMN lesions

A

Stroke,
Multiple Sclerosis, Spinal cord damage, Cerebral palsy (has S sound)
Spastic paralysis
Upward Babinski (towards the Sky)
Strong muscles (little to no muscle atrophy

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4
Q

FLABBY LMN lesions

A

Fasciculations present
Loss of muscle tone
Areflexia (hypotonic)
Babinski towards the Basement (downwards)
Young (poliomyelitis is known as infantile paralysis)
LMN: Remember the B’s of LMN lesions!!!
Etiologies: Guillain Barré syndrome, Botulism, Back pain due to Cauda Equina syndrome, Bell Palsy, Baby paralysis (Polio)
Loss of muscle tone/Flaccid paralysis and muscle atrophy

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5
Q

riluzole

A
  • only drug for ALS
  • MOA: Unknown, inhibits Glutamate release
  • S/E: Weakness and Nausea
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6
Q

Baclofen

A
  • MOA: Inhibits transmission of reflexes at the spinal cord leading to resolution of spasticity
  • S/E: Hypotonia, Drowsiness
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7
Q

atropine

A

MOA: ???anticholinergic

S/E ????tachy, pupil dilation, etc

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8
Q

muscle contraction score

A

0-No muscle contraction

1-Trace-muscle contraction

2-Limb movement with gravity eliminated

3-Limb movement against gravity

4-Power decreased but possible against resistance

5-Normal power

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9
Q

how does drug induced myopathy present

A

Slow onset of weakness days to months. Progressive weakness, myalgia and fatigue

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10
Q

best dx test for drug induced myopathy

A

creatine kinase

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11
Q

how does neuropathic pain present

A

A burning, shooting “electric shock” like pain

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12
Q

when does idiopathic trigeminal neuralgia usually present?

A

Idiopathic usually occurs in 6th decade

Must r/o MS if it happens to young patient

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13
Q

what do you have to r/o if somebody has trigeminal neuralgia

A

MS

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14
Q

how to treat trigeminal neuralgia

A

carbamazepine
MOA: Limits influx of sodium ions across cell membranes. Also has Anticholinergic, Antineuralgic, Antidiuretic, and Antiarrhythmic properties
S/E: Dizziness, Nausea Vomiting
Can also lead to ???SIADH

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15
Q

if carbamazepine doesn’t work for TGN then try….

A

MICROVASCULAR DECOMPRESSION

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16
Q

PE findings for occipital neuralgia

A

Occipital nerve tender to palpation
+ Tinel sign (tapping nerve)
Numbness in the nerves skin distribution

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17
Q

how to tx occipital neuralgia

A

Nerve block with Lidocaine and Steroid diagnostic and curative

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18
Q

how to manage post-herpetic neuralgia

A

TCA: Amitriptyline, Nortryptiline
Gabapentine
May use Opioids for severe pain

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19
Q

hpyeractive delirium
hypoactive
mixed

A

Hyperactive: Usually due to ETOH withdrawal, intoxication or drug abuse (LSD, PCP)
Hypoactive: Usually seen in patients with Hepatic encephalopathy and Hypercapnia
Mixed: Daytime sedation with nocturnal agitation and behavioral problems (sundowning)

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20
Q

clinical manifestations of delirium

A

Acute confused state, rapid onset with fluctuating mental status changes.
Visual hallucinations, Grandiose delusions, suicidal ideation.
Dysphagia, Dysarthria, Tremor, & Motor Abnl

21
Q

MC tx for delirium

A

haldol (anti-dopamine)

EPS/tardive dyskinesia are common with these

22
Q

MC type of dementia

A

alzehimers (gold standard for detection is an autopsy)

23
Q

3 hypothesis for alzheimer’s

A
  • Amyloid hypothesis-amyloid deposits (senile plaques)
  • Tau protein hypothesis-neurofibrillatory tangles (tau proteins)
  • Cholinergic Deficiency hypothesis (cerebral cortex atrophy)
24
Q

how to manage alzheimer’s

A

-donapezil, rivastigmine
MOA- achase inh, increase ach

-memantine
MOA-NMDA antagonist → Slows calcium influx & nerve damage. Glutamate is an excitatory neurotransmitter of the NDMA receptor. Excitotoxicty causes cell death.
Memantine blocks Receptor

25
Q

2nd MC type of dementia

A 
vascular
Lacunar infarcts (seen on CT) are due to chronic ischemia

Most commonly associated with longstanding HTN

26
Q

Pick’s disease

A
  • Degeneration of the brain in the Frontotemporal area but may progress to whole brain
  • This presents with personality change FIRST and occurs before memory loss
  • seen in old age
27
Q

Lewy-Body dementia

A

Lewy bodies are smooth round protein lumps which are found in the nerve cell of the affected brain
-Differentiated from other dementias by Visual hallucinations, orthostatic hypotension, and parkinsonism (Parkinson like sympoms but not substantia nigra damage)

28
Q

Huntington’s disease

A

-Autosomal dominant disease affecting 8/100,00 people
Neurodegenerative disorder  Cerebral and Caudate nucleus atrophy
-Father or mother had a history of……mom or dad passing away early

29
Q

How does Huntington’s present

A

Behavioral changes, then chorea, then dementia

Similar to picks disease but these pts are younger such as 35

30
Q

HA for 3-4 weeks, 60-70 YO s/p fall

CT shows gray instead of white

A

chronic subdural hematoma, tx w/tylenol

31
Q

Rare autosomal recessive inherited disorder of copper metabolism  Deposition of copper in the liver, brain, and other tissues

A

Wilson’s disease

accumulates in liver leading to cirrhosis

32
Q

how does Wilson’s present

A

Difficulty speaking, salivation, ataxia, clumsiness with hands, and personality changes
Dystonia, spasticity, seizures, rigidity, and flexion contractures.
Keyser Fleischer rings
CT SCAN: Giant panda sign

33
Q

how to tx Wilson’s disease

A

TRIENTINE
MOA:Copper chelator
SE: bone marrow suppression, proteinuria, Fe def anemia
CBC weekly when treated

34
Q

you have to r/o MS for these 3 conditions

A

trigeminal neuralgia
Pain in eye, diplopia, pupil dilates and doesn’t constrict
Optic neuritis

35
Q

MS patho

A

Demyelination —> scarring & hardening of nerve fibers usually in the spinal cord, brain stem and optic nerves* —> Slow nerve impulses weakness numbness pain and vision loss.

36
Q

MC neurological cause of debilitation in young people

A

MS

37
Q

primary progressive MS

A

Less common form of MS leads to gradual decline w/o remission.
US >40 when symptoms begin (pt presents later, gets worse and worse)

38
Q

secondary progressive MS

A

More than ½ people with relapsing remitting MS eventually enter a stage with continuous deterioration.

39
Q

Relapsing-remitting MS

A
  • MC type
  • Characterized by clearly defined flare-ups periods of remission.
  • Flare-ups appear suddenly, last a few weeks or months, and than disappear
40
Q

clinical signs of MS

A

-weakness, fatigue, spasticity (UMN)

-Uhthoff’s Phenomenon:
Worsening of symptoms with heat (sauna, marathon)

-Lhermitte’s Phenomenon:
Lightening shock pain shooting from spine down the leg with neck flexion

41
Q

25 YO female, right eye pain, photophobia,
If pain is gone with tetracaine it is corneal abrasion
If it still hurts after tetracaine think optic neuritis you must r/o

A

MS

Marcus gunn pupil will present (above picture)

42
Q

3 phenomena associated with optic neuritis

A

Flashes of light usually with eye movements

Worsening symptoms (deterioration of vision) induced by exercise, hot meal, or hot bath

Pulfrich effect- sense of disorientation in moving traffic

43
Q

Charcot’s neuralgic triad

A

Intentional tremor (happens with intent)
Nystagmus
Stacatto Speech

44
Q

how to dx MS

A

-MRI with Gadolinium
-Hyperdensities (Plaques) affecting white matter
Must have 2 or more areas of white matter involved before dx is made
-CSF Increased IGG Oligoclonal Bands

45
Q

how to manage MS

A

-prednisone
-MOA: Weakens immune system by suppression of migration of PMN leukocytes and reversal of increased capillary permeability
SE: weakened immune system, adrenal suppression, hyperglycemia

46
Q

how to manage relapsing-remitting MS

A

B-Interferon -Immunosuppressant

Glatiramer -Synthetic compound made up of four amino acids that are found in myelin. Stimulates T cells in the body’s immune system to change from harmful, pro-inflammatory agents to beneficial, anti-inflammatory agents that work to reduce inflammation at lesion sites

47
Q

Gilenya

A 
New class of medication called a sphingosine 1-phosphate receptor modulator, which is thought to act by retaining lymphocytes, thereby preventing those cells from crossing the blood-brain barrier into the (CNS). Preventing the entry of these cells into the CNS reduces inflammatory damage to nerve cells.
Monitor 1st dose due to bradycardia
48
Q

natalizumab

A

Monoclonal antibody. It is designed to hamper movement of potentially damaging immune cells from the bloodstream, across the “blood-brain barrier”

Neuro 2 (2 decks)

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