Brain stuff

Question 1

ALS

Answer 1

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

Question 2

how does ALS present

Answer 2

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

Question 3

S of UMN lesions

Answer 3

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

Question 4

FLABBY LMN lesions

Answer 4

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

Question 5

riluzole

Answer 5

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

Question 6

Baclofen

Answer 6

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

Question 7

atropine

Answer 7

MOA: ???anticholinergic

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

Question 8

muscle contraction score

Answer 8

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

Question 9

how does drug induced myopathy present

Answer 9

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

Question 10

best dx test for drug induced myopathy

Answer 10

creatine kinase

Question 11

how does neuropathic pain present

Answer 11

A burning, shooting “electric shock” like pain

Question 12

when does idiopathic trigeminal neuralgia usually present?

Answer 12

Idiopathic usually occurs in 6th decade

Must r/o MS if it happens to young patient

Question 13

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

Answer 13

MS

Question 14

how to treat trigeminal neuralgia

Answer 14

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

Question 15

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

Answer 15

MICROVASCULAR DECOMPRESSION

Question 16

PE findings for occipital neuralgia

Answer 16

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

Question 17

how to tx occipital neuralgia

Answer 17

Nerve block with Lidocaine and Steroid diagnostic and curative

Question 18

how to manage post-herpetic neuralgia

Answer 18

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

Question 19

hpyeractive delirium
hypoactive
mixed

Answer 19

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)

Question 20

clinical manifestations of delirium

Answer 20

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

Question 21

MC tx for delirium

Answer 21

haldol (anti-dopamine)

EPS/tardive dyskinesia are common with these

Question 22

MC type of dementia

Answer 22

alzehimers (gold standard for detection is an autopsy)

Question 23

3 hypothesis for alzheimer’s

Answer 23

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

Question 24

how to manage alzheimer’s

Answer 24

-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

Question 25

2nd MC type of dementia

Answer 25

``` vascular Lacunar infarcts (seen on CT) are due to chronic ischemia ``` Most commonly associated with longstanding HTN

Question 26

Pick's disease

Answer 26

- 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

Question 27

Lewy-Body dementia

Answer 27

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)

Question 28

Huntington's disease

Answer 28

-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

Question 29

How does Huntington's present

Answer 29

Behavioral changes, then chorea, then dementia | Similar to picks disease but these pts are younger such as 35

Question 30

HA for 3-4 weeks, 60-70 YO s/p fall | CT shows gray instead of white

Answer 30

chronic subdural hematoma, tx w/tylenol

Question 31

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

Answer 31

Wilson's disease | accumulates in liver leading to cirrhosis

Question 32

how does Wilson's present

Answer 32

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

Question 33

how to tx Wilson's disease

Answer 33

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

Question 34

you have to r/o MS for these 3 conditions

Answer 34

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

Question 35

MS patho

Answer 35

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.

Question 36

MC neurological cause of debilitation in young people

Answer 36

MS

Question 37

primary progressive MS

Answer 37

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

Question 38

secondary progressive MS

Answer 38

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

Question 39

Relapsing-remitting MS

Answer 39

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

Question 40

clinical signs of MS

Answer 40

-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

Question 41

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

Answer 41

MS | Marcus gunn pupil will present (above picture)

Question 42

3 phenomena associated with optic neuritis

Answer 42

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

Question 43

Charcot's neuralgic triad

Answer 43

Intentional tremor (happens with intent) Nystagmus Stacatto Speech

Question 44

how to dx MS

Answer 44

-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

Question 45

how to manage MS

Answer 45

-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

Question 46

how to manage relapsing-remitting MS

Answer 46

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

Question 47

Gilenya

Answer 47

``` 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 ```

Question 48

natalizumab

Answer 48

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