Neuro Week 4

Front 1

How do neuromuscular blockers work?

Back 1

They bind to ACh nicotinic receptors on the muscle and block reflex.

Front 2

How do non-depolarizing neuromuscular blockers work?

Depolarizing?

Back 2

The non-depolarizing blockers work by competitively inhibiting ACh at the neuromuscular junction.

The depolarizing blockers work by permanently depolarizing the post-synaptic cells at the neuromuscular junction.

Front 3

What is the intrinsic activity of non-depolarizing neuromuscular blockers?

Back 3

They have no intrinsic activity because they have no effect on the post-synaptic cell.

Front 4

What is tubocurarine?

Back 4

Tubocurarine is a non-depolarizing neuromuscular blocker.

Front 5

When a non-depolarizing neuromuscular blocker is used, how much ACh binds nicotinic receptors?

Back 5

Since inhibition is competitive, some ACh will still bind the nicotinic receptor, but it will not reach the threshold for contraction.

Front 6

How is the action of a non-depolarizing neuromuscular blocker reversed?

Back 6

With the use of AChE inhibitor- ACh levels will rise and outcompete the blocker for binding to nicotinic receptors.

Front 7

Which type of cholinesterase inhibitor is a more effective agent to reverse the action of non-depolarizing neuromuscular blocker?

Back 7

Quarternary amines like neostigmine are best because they will prevent breakdown of ACh and have some agonist action on the nicotinic receptor.

Front 8

Which nicotinic receptors are affected by neuromuscular blockers?

Back 8

Neuromuscular only, not ganglionic

Front 9

What is the most commonly used depolarizing neuromuscular blocker?

Back 9

Succinylcholine

Front 10

What molecule metabolizes succinylcholine?

What is the effect of using a cholinesterase inhibitor?

Back 10

Cholinesterase

Use of cholinesterase will enhance the effects of succinylcholine because the succinylcholine will not be broken down.

Front 11

How does succinylcholine act?

Back 11

1. Binds to nicotinic receptor
2. Depolariziation (fasciculations)
3. Repolarization block
4. Muscle paralysis

Front 12

In what sort of patients should succinylcholine not be used? Why?

Back 12

Burn patients, because succinylcholine increases the amount of potassium released into the plasma and may cause cardiac arrest.

Front 13

What is the effect of a muscarinic blocker on the eye, lacrimal gland, salivary glands, heart, lung, GI tract, bladder, and penis?

Back 13

In general sympathetic effects

Front 14

What is atropine?

Back 14

A competitive antagonist of muscarinic receptors that binds to all five types of receptors.

Front 15

What are the therapeutic uses of atropine?

Back 15

Eye exam (dilation)
Pre-anesthetic medication (inhibition of salivary and bronchial secretion, bronchodilation)
Treatment of bradycardia
Treatment of hyper-hydrosis
Treatment of irritable bowel syndrome with diarrhea

Front 16

What are the symptoms of atropine poisoning?

Back 16

Hyperthermia
Salivary and lacrimal glands dry up
Hallucinations
Constipation
Blurred vision
Photophobia
Tachycardia
Difficulty urinating
Penile flaccidity

Front 17

How is atropine poisoning treated?

Back 17

Wait it out- half life is 4 hours

Cholinesterase inhibitor will increase ACh levels so ACh can compete for binding

Front 18

How does botox work?

What are some non-cosmetic uses?

Back 18

It prevents ACh release from neurons, preventing muscle contraction.

Unbalanced ocular muscles
Uncontrolled blinking
Excessive axillary sweating
Failure of esophagel sphincter to relax

Front 19

How can you tell the difference between botox and atropine poisoning?

Back 19

Atropine does not cause skeletal muscle weakness, while botox does.

Cause of death by botox is respiratory failure, while with atropine it is hyperthermia.

Front 20

What is the striatum?

Back 20

Putamen + caudate

Front 21

What are the three hypokinesias? Define them.

Back 21

1. Bradykinesia: slow movement
2. Akinesia: complete lack of movement
3. Rigidity: increased muscle tone

Front 22

What are the five hyperkinesias? Define them.

Back 22

1. Tremor: oscillatory, rhymical, regular movement of one or more body parts. Can be classified as rest, posture, or action.
2. Chorea: involuntary, irregular, purposeless, non-rhythmic, rapid, jerky movements that flow from one body part to another. Choreoathetosis is chorea with athetosis, which is a slow, writhing movement.
3. Dystonia: systained, involuntary, abnormal posturing. Can be classified as focal, segmental (contiguous parts), or generalized (leg + other).
4. Myoclonus: sudden, brief, twitch-like involuntary movement. Can arise from injury to cortex, brainstem, or spinal cord.
5. Tics: semi-voluntary, repetitive, intermittent, stereotypic movements or sounds.

Front 23

Name some causes of parkinsonism other than idopathic Parkinson's disease.

Back 23

1. Medication
2. Infection
3. Vascular disease
4. Other neurologic disease

Front 24

What are the cardinal symptoms of idiopathic Parkinson's disease?

What are some associated features?

Back 24

Cardinal: TRAP- tremor (rest), rigidity, akinesia, postural instability

Associated: assymetric onset, hypophonia, hypomimia, bradyphrenia, micrographia, gait abnormality, stooped/flexed posture

Front 25

Physiologically, what is responsible for Parkinson's disease?

Back 25

Loss of dopamine-containing neurons in the substantia nigra pars compacta. Lewy bodies can be seen in SNpc neurons.

Front 26

What is the most effective treatment for parkinsonism?

What are some drawbacks of this treatment?

Back 26

Levodopa (L-DOPA)
Sinemet: carbidopa + levodopa (carbidopa inhibits plasma dopa decarboxylase)

Nausea, orthostatic dizziness, sedation, confusion, hallucination, motor fluctuations

Front 27

A 72 year old man presents with hand tremor for the past 20 years. He states his tremor bothers him most when he is using his hands, eating, and writing. He has no bradykinesia, gait, or balance difficulties. He also has a voice tremor when he speaks. What is the most likely diagnosis?

Back 27

Essential tremor

Front 28

Damage to what structure is associated with intention tremor?

Back 28

Cerebellum

Front 29

Describe the clinical features of essential tremor.

Back 29

Occurs in upper extremity, head, speech, tongue, trunk, or lower extremities. It is an action tremor. There is no other neurologic abnormality. 60% of the time one drink will calm the tremor. Onset at any age. 60% have family history (autosomal dominant- incomplete penetrance)

Front 30

A 40 year old man presents with depression starting in his 20's. He then developed memory impairment and started to have twitching of his muscles. His maternal grandfather had similar movements, and his mother was asymptomatic but committed suicide at age 35. What is the most likely diagnosis?

Back 30

Huntington's disease

Front 31

What is the clinical triad of Huntington's disease?

Back 31

1. Psychiatric
2. Cognitive (dementia)
3. Movement disorder (chorea)

Front 32

Describe the pathophysiology of Huntington's.

Back 32

Caudate atrophy

Front 33

Describe the inheritance of Huntington's disease.

Back 33

Autosomal dominant
100% penetrance
Triplet CAG repeat on chr 4 (more repeats, more severe)

Front 34

A 54 year old woman presents with sudden onset of R arm flinging movements. She has a history of poorly controlled diabetes and HTN. There is a lesion on the STN. What is the most likely diagnosis?

Back 34

Hemiballism

Front 35

Describe hemiballism.

Back 35

Involuntary large amplitude flinging limb movements affecting one side. Often associated with contralateral STN lesion from hemorrhage or stroke.

Front 36

A 47 year old man presents with 9 months of progressive L neck pulling. He now has a painful L head tilt and L shoulder elevation. He cannot drive and has difficulty sleeping because of pain. He has no other symptoms. What is the most likely diagnosis?

Back 36

Cervical dystonia

Front 37

Describe primary generalized dystonia.

Back 37

Childhood onset in limb with gradual progression over years to involve limbs, pelvis, trunk, neck. Mentation is spared. Autosomal dominant with incomplete penetrance and common in Ashkenazi Jews. Due to mutation in DYT1. Can be treated with deep brain stimulation.

Front 38

Describe focal dystonia.

Back 38

Develops in adulthood and is idiopathic. Unlikely to spread. Alleviated by sensory tricks. Treated with botox, anticholinergics, benzodiazepines, or baclofen.

Front 39

A 21 year old man complains of an urge to move his scalp. He feels an itch taht goes away when he moves the scalp, but then the urge builds up again. He also has occasional nose sniffing that was diagnosed as seasonal allergies. What is the most likely diagnosis?

Back 39

Tic disorder

Front 40

What are the diagnostic criteria, associations, and treatments for Tourette syndrome?

Back 40

Criteria:
Onset before age 21
Both phonic and motor tics
Tics present for 12+ months

Associations:
ADHD
OCD

Treatment:
Neuroleptics (may cause tardive syndrome)
Clonazepam
Clonidine

Front 41

A 56 year old woman with history of bipolar disorder presents with 10 years of oral-buccal-lingual movements. She has a history of neuroleptic exposure for many years. She also has some parkinsonism and tremor. What is the most likely diagnosis?

Back 41

Tardive dyskinesia

Front 42

What is tardive dyskinesia?

Back 42

A syndrome appearing after use of dopamine antagonists like neuroleptics and antiemetics. Oral/buccal movements are most common. Develops over years.

Other tardive syndromes may develop on a different time frame, but have different symptoms like parkinsonism, restlessness, etc.

Front 43

What is myoclonus?

Back 43

Sudden, brief jerks.

Positive: brief contractions
Negative: brief lapses in posture

It is a symptom often present in other movement disorders.