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Neuro Flashcards

1
Q

How to ID horizontal axis in the CNS

A
  1. Hyperreflexia
  2. Spasticity: VELOCITY-dependant (need to go fast) “catch” with rapid passive extension of joint
  3. Sensory changes: often harder to localize*
  4. Weakness
  5. Upper Extremity
    - Greater weakness of extensor muscles
    - Flexor posturing, pronator drift
  6. Lower Extremity
    - Greater weakness of flexor muscles
    - Extensor posturing, circumduction of leg with gait
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2
Q

How to ID horizontal axis in the PNS

A
  1. Hypo-reflexia
  2. Atrophy/Fasciculation
  3. Sensory changes
  4. Dermatomal: Radiculopathy
    - Sensory nerve distribution: Mononeuropathy
    - Glove/Stocking: Polyneuropathy (starts distally and move proximally)
  5. Weakness
    - Unilateral: often focal/single muscle group affected
    - Bilateral: generally greater either proximally or distally
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3
Q

How to ID vertical axis in the CNS

A
  1. Unilateral vs bilateral sx
    - Unilateral symptom:
  2. Could be from any level but think cortex/brainstem first.
  3. Spinal cord less likely due to narrow cross sectional area.

Bilateral symptom:

  1. NOT caused by a cortical lesion.
  2. Lesion could be subcortical, brainstem, or spinal cord
  3. Part of body affected
    - ie: face, upper extremity, lower extremity (or a combination).
    - The lesion could be anywhere “upstream” from the most proximal affected area.
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4
Q

How to ID vertical axis in the PNS

A
  1. Pay attention to reflexes
  2. Achilles: S1/S2
  3. Patellar: L3/L4
  4. Biceps: C5/C6
  5. Triceps: C7/C8
  6. Dermatomes!
  7. Muscle innervations
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5
Q

What is MS

A

-Episodic demyelinating events of central nervous system (brain +/- spinal cord)- Axonal damage causes persistent symptoms

-Neurodegeneration (cell death) -
Causes brain to atrophy up to 3x faster than normal.

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6
Q

Describe the epidemiology of MS

A
  1. F>M
  2. 15-45
  3. Latitude: Increasingly common as you travel further away from the Equator
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7
Q

Risk factors for Ms

A
  1. Genetics
  2. Personal Hx of autoimmune conditions
  3. Vitamin D deficiency
  4. Viral infections: Epstein-Barr, Varicella, Cytomegalovirus
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8
Q

Describe the subtypes of MS

A
  1. Relapse- -Result from acute demyelinating events
    - Normally cause new symptoms
  2. Progression –Due to a combination of incomplete healing after relapses and progressive atrophy of brain/cord.
    - Most patients eventually develop progressive disease.
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9
Q

Describe the possible presenting sx of MS (differs based on lesion location)

A
  1. Parasthesias
  2. Weakness
  3. Spasticity
  4. Ataxia
  5. Vertigo
  6. Urinary/Bowel hesitancy or urgency
  7. Vision changes: diplopia, decreased color saturation, painful eye movement, visual field deficits.
  8. Other cranial nerve abnormalities
  9. Severe fatigue
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10
Q

Describe laters sx of MS that appear w/ disease progression

A
  1. Gait impairment/ feeling feet are very heavy
  2. Imbalance
  3. Cognitive Impairment
  4. Sleep impairment
  5. Easy fatigability with physical activity
  6. Depression
  7. Sexual dysfunction
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11
Q

Describe the PE Of MS

A
  • Sometimes exam will be normal. Not all symptoms have associated signs on exam.
    1. Use “horizontal” and “vertical” axes to help determine location of new lesions and focus imaging. (CNS SX!)

Possible abnormal findings:

  1. Motor: Weakness in CNS pattern, spasticity
  2. Reflexes: Hyperreflexia, clonus, up-going Babinski sign
  3. Cerebellar: tremor, ataxia, nystagmus, dysarthria
  4. Sensory: impaired vibratory/pain/light touch sensation, allodynia
  5. Cranial nerves: afferent pupillary defect, impaired EOMs, facial asymmetry, sensory changes
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12
Q

Tx options for MS

A
  • Goes is disease modification and reduce progression NOT Healing
    1. Disease modifying therapy
    2. Vit. D goal 50-100
    3. HD Steroids 3-5 days (acute tx of relapse,– get better faster, not better better!)

*Ongoing research looking at medications to treat progressive disease/atrophy and improve re-myelination following a relapse.

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13
Q

mechanism for MS meds

A
  1. Blockade of blood-brain barrier
  2. Sequestration of lymphocytes in lymph nodes
  3. Prevention of rapid lymphocyte replication
  4. Modulation of T-cell subtypes
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14
Q

How do you manage the sx of MS

A
  1. Meds- Be careful not to overmedicate. Most medications with CNS targets can cause sedation, cognitive impairment, imbalance, etc.
  2. PT (ongoing)- compensate better for neuro impairments and reduce deconditioning
  3. Smoking cessation
  4. Assistive device for ambulation

*Goal is functional improvement, not symptom resolution.

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15
Q

What is the important “coordination center” for movement

A

basal ganglia- Cluster of nuclei in the subcortical grey matter

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16
Q

the basal ganglia has connections to:

A
  1. cortex
  2. thalamus
  3. brainstem
  4. cerebellum

*All efferent and afferent neurons from you brain come together at the basal ganglia

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17
Q

Smaller and slowness of movement execution, often with reduced movement amplitude

A

Bradykinesia

*often seen in parkinsons

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18
Q

increased muscle tone in both agonist and antagonist muscles, not velocity-dependent

A

Rigidity

stiffer- harder to flex, test w/ elbows and ankles

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19
Q

rhythmic muscle contraction/relaxation causing oscillating movement

A

Tremor

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20
Q

internal restlessness and need to move

A

Akathisia

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21
Q

irregular, discrete and often sequential* involuntary movement

A

Chorea

dance like movement

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22
Q

slow, involuntary, writhing movement. A type of slow chorea

A

Athetosis

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23
Q

patterned, twisting movement caused by intermittent or sustained muscle contraction. Often initiated or worsened by voluntary movement*

A

Dystonia

torsional component

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24
Q

brief, intermittent, stereotyped movements associated with urge to make the movement

A

Tics

*can suppress it for a little but eventually have to do it

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25
Q

Tremor subtypes

A
  1. Essential tremor
  2. Parkinsonian tremor
  3. Cerebellar tremor
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26
Q

Describe an essential tremor

A
  1. Worsens with posture and/or activity– bringing hand torwards faces
  2. Can be low or high amplitude
  3. May begin unilaterally or bilaterally
  4. Worse w/ holding a weight
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27
Q

Describe a Parkinsonian tremor

A
  1. Rest tremor, improves with purposeful movement
  2. “Pill-rolling tremor”, generally 4-6 Hz
  3. Begins unilaterally in Parkinson’s disease (may be bilateral in other forms of parkinsonism)
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28
Q

Describe a cerebellar tremor tremor

A
  1. Occurs at the end of intentional movement** (Intention tremor– gets worse at the end of the initial movement–> test w/ finger to nose test)
  2. Slow, broad tremor with large amplitude/ “flapping component”
  3. Often associated with ataxia
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29
Q

Describe the pathophysiology of Parkinson’s

A

Gradual depletion of dopamine due to progressive loss of dopaminergic neurons in the substantia nigra

**Diminished substantia nigra

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30
Q

Lewy body plaques seen on autopsy

A

Parkinson’s

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31
Q

Motor sx onset in Parkinson’s is typically begins when

A

~10 yrs after this degenerative process begins

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32
Q

Possible triggers for the degenerative process of Parkinson’s

A
  1. Genetics
  2. toxin exposure (ie. pesticides, mines, agent orange)
  3. head trauma.

*The majority of cases are considered idiopathic at this point.

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33
Q

Describe the epidemiology of Parkinsons

A
  1. increase w/ age (most over 40)
  2. M>F slightly
  3. Genetics
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34
Q

Describe the initial sx of Parkinson’s

A
  1. Symptoms begin unilaterally but can progress to contralateral side.
  2. Symptoms progress slowly over time. Not all patients develop every symptom.
  3. Motor sx
  4. Bradykinesia
  5. Rigidity
  6. Tremor
  7. Gait impairment
  8. REM Sleep disorder (movement in sleep), insomnia
  9. impaired sense of smell
  10. Constipation

(8-10 often predate motor sx by many yrs)

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35
Q

Describe the motor sx of Parkinsons

A
  1. Bradykinesia: masked facies, decreased spontaneous movement, reduced arm swing with gait
  2. Rigidity: impairment in fine motor tasks, gait, fatigability
  3. Tremor: rest “pill rolling” tremor. SOME PATIENTS DO NOT HAVE TREMOR!
  4. Gait impairment: shuffling, festination/freezing, pedestal turning
    - Hunched, short steps, no arm swings
    - Commonly one foot stomp or only 1 arm swing
36
Q

What are advanced sx of Parkinson’s disease

A
  1. Increased gait instability and falling
  2. Cognitive impairment +/- dementia
  3. Visual hallucinations
  4. Depression** (low dopamine- but may be masked facies too)
  5. Hypophonia and dysarthria
  6. Autonomic dysfunction

These symptoms are typically poor responders to dopaminergic medications and are often exacerbated by them. Medical management of advanced Parkinson’s is a balancing act.

37
Q

Sx of autonomic dysfunction seen w/ advanced Parkinson’s

A
  1. Orthostatic hypotension* (fall a lot– feel better sitting down)
  2. Constipation
  3. Swallowing dysfunction
  4. Poor temperature regulation
38
Q

Common SE of Parkinson’s meds

A

These medications have many side effects

  1. fatigue
  2. nausea,
  3. sleep disturbance,
  4. psychosis,
  5. orthostatic hypotension, etc.)
39
Q

Tx of Parkinsons

A
  1. Meds- Most have short half lives and require dosing at least three times daily
  2. PT

*VERY IMPORTANT to include ongoing physical therapy and counsel about assistive devices for ambulation/balance (walker and/or trekking poles are much safer than a cane).

40
Q

Meds used in Parkinsons

A
  1. Levadopa
  2. Dopamine agnonists (pramipexole, ropinerole):
  3. Entacapone
  4. MAOB-inhibitor(selegiline, rasagline)
  5. Amantadine
  6. Anti-cholinergics

*best to use low dose of multiple drugs vs HD of 1 med (rational polypharmacy)

41
Q

Describe deep brain stimulation used in parkinsons

A

Leads implanted in the sub-thalamic nuclei of the basal ganglia.
Uses electric current to help “correct” the impaired feedback loops resulting from lack of dopamine.

42
Q

Deep brain stimulation is a possible thearpy for pts w/ Parkinsons with:

A

Leads implanted in the sub-thalamic nuclei of the basal ganglia.
Uses electric current to help “correct” the impaired feedback loops resulting from lack of dopamine.

Most beneficial for motor symptoms. Does not improve postural instability, autonomic dysfunction, speech impairment.

43
Q

Describe the characteristics of essential tremor

A
  1. Typically bilateral of upper extremities
  2. Progressive over years/decades
  3. Postural and/or kinetic. Not present at rest
  4. May also be present in face, voice
  5. 4-10 Hz (faster than parkinsonian tremor)
  6. Classically improves with alcohol**

*VERY strong genetic link (M=F_

44
Q

Tx of Essential tremor

A
  1. Medications: Beta-blockers (propranolol), anti-convulsants (primidone)
  2. Deep brain stimulation for disabling tremor that is resistant to medications
45
Q

Characteristics of restless leg syndrome

A
  1. Unpleasant sensations in lower extremities associated with urge to move.
  2. IMPROVED WITH STANDING/WALKING
  3. Typically begins in the evening or at bedtime.
  4. Often associated with periodic limb movement (a sleep disorder)
  5. often caused by iron deficiency or w/ other underlying neuro conditions
46
Q

TX of restless leg syndrome

A
  1. Iron replacement if indicated

Medications

  1. Dopamine agonists (pramipexole, ropinerole)
  2. Anti-convulsants (gabapentin, pregabalin)
  3. Opioids (codeine)
47
Q

Describe common sx in Huntington’s disease

A
  1. Progressive neurodegenerative disease (100% fatal)
  2. Chorea (progressive)
  3. Psychiatric sx
  4. Dementia- Prominent executive functioning impairment
  5. Chorea replaced by akinesia and rigidity
  6. Weight loss and cachexia
  7. Death typically 10-30 years after symptom onset
48
Q

Describe the psychiatric sx seen in Huntington’s

A
  • Common: depression, anxiety, irritability, apathy
  • Less common: OCD, psychosis
  • Increased rate of suicidal ideation
49
Q

Describe the genetic component of Huntingtons

A

**Autosomal dominant
-Increased number of CAG repeats on chromosome 4
100% penetrance with 40+ CAG repeats

greater number of CAG repeats= earlier onset

Obtaining detailed family history is important (can’t rule out positive FHx if family member died early of other causes)

50
Q

Describe the Management of Supportive care

A
  1. Supportive Care
  2. Physical/Occupational Therapy
  3. Tetrabenazine for chorea
  4. Speech therapy to address swallowing
  5. Psychiatric management
  6. High calorie diet
  7. Consideration of feeding tube for aspiration
  8. Family planning/genetic testing
51
Q

What is a nerve conduction study

A

-Utilizes a small amount of electric current between two electrodes to tell you were entrapment is!!

  • Non-invasive but can be painful
  • Measures both latency and amplitude of peripheral and sensory peripheral nerve fibers
  • Normal in CNS disorders!
52
Q

Describe the workup of radiculopathy

A
  1. Consistent exam: motor, sensory, reflexes
  2. Nerve conduction study: may show diminished action potential (IF you can get an electrode on either side of the lesion)
  3. MRI of appropriate spine level
53
Q

Describe the managment of radiculopathy

A
  1. Steroid injections
  2. PT to address associated muscle spasming/weakness
  3. Pain medications: start with neuropathic pain meds (anti-epileptics, TCAs, SNRIs), not opioids. NSAIDs sometimes helpful if arthritic component.
  4. Surgery (need to have failed steroids)
54
Q

Radiculopathy is typically due to

A
  • foraminal narrowing
    1. Degenerative disc disease
    2. Osteoarthritis
    3. Spondylolisthesis (anterior or posterior displacement of a vertebra)

*Injury/enrapment of nerve root

55
Q

Describe the presentation of radiculopathy

A
  1. Typically unilateral (or more severe on one side)
  2. Sensory change/pain in dermatomal pattern
  3. Normally associated neck or back pain
  4. Weakness in muscles innervated by that nerve root.
56
Q

Describe the work up of mononeuroapthies

A
  1. Nerve conduction study: prolonged latency across point of compression
  2. MRI: can be helpful in establishing point of compression if this is unclear
57
Q

Describe the tx of mononeuroapthies

A
  1. Start with conservative management unless atrophy is already present
    2, Steroid injections
  2. Bracing to reduce compression
  3. Surgical decompression
    -Indicated for progressive symptoms, particularly increased weakness and/or atrophy***
    -Sensory changes generally improve, weakness and atrophy may not
    -Don’t delay too long if indicated
58
Q

What is Bell’s Palsy

A
  • Peripheral mononeuropathy of Cranial Nerve VII
  • Inflammation of nerve causes compression at the stylomastoid foramen

*no facial expression problems

59
Q

causes of Bell’s Palsy

A

Cause unknown, may be related to viral infection such as Epstein-Barr or varicella zoster

60
Q

Describe the workup of Bell Palsy

A
  1. Consistent physical exam
  2. MRI brain w/wo contrast to rule out other causes. May see enhancement of CN VII
  3. Diagnosis of exclusion. Rule out other possible causes of CN VII palsy (stroke, tumor, meningitis, sarcoidosis, diabetes mellitus, head trauma)
61
Q

Describe the management of Bell’s Palsy

A
  1. Typically acyclovir and prednisone although no clear evidence that these help.
  2. Taping of eyelid for sleep, lubricant eye drops as needed
  3. Gradual recovery, complete resolution of symptoms in 2/3 of patients at one year.
62
Q

How do you tell the difference between Stroke vs Bell Plasy

A

forehead involvment- peripheral nerve (likely Bell Palsy)

No forehead involement: likely a stroke (central)

63
Q

Describe sx of peirphearl polyneuropathy

A
  1. Symmetric
  2. Fiber-length dependent (symptoms appear in feet before hands, travels proximally over time)
  3. Sensory changes
  4. Motor changes- Generally starts with weakness of dorsiflexion/atrophy of foot muscles (high arch)
64
Q

Describe the sensory changes w/ peripheral polyneuropathy

A
  1. Paresthesia, numbness, allodynia
  2. Glove and stocking pattern, sparing of torso
  3. Vibration and temperature sensory loss typically precede pinprick and light-touch loss
65
Q

Describe the work up peripheral polyneuropathy

A
  1. Symmetric hypo-reflexia and sensory changes greatest distally, +/- weakness/atrophy
  2. Positive Romberg testing (cannot feel the ground)
  3. Consistent nerve conduction studies
  4. Family history: can be hereditary, especially if earlier age of onset.
  5. Labwork
66
Q

Describe the labwork of peripheral polyneuropathy

A

*Many, many causes of peripheral neuropathy. Most are not treatable or reversible.

Focus on common and possibly correctable etiologies such as:

  1. Hgb A1c (MOST COMMON CAUSE!)
  2. Vitamin deficiencies (Vitamin D, Vitamin B12)
  3. TSH
  4. SPEP (serum protein immunofixation)
67
Q

Describe the managment of peripheral polyneuropathy

A
  1. Treatment of reversible etiologies if possible
  2. Medications to address pain (not very helpful for addressing numbness)
  3. Physical therapy, assistive devices, night lights, etc
68
Q

Define Guillain Barre

A
  • Inflammatory (demyelinating) peripheral neuropathy
  • 2/3 of cases preceded by infection (most common: Campylobacter jejuni)
  • autoimmune
69
Q

Describe the sx of Guillian barre

A
  1. Progressive weakness over 1-2 weeks (relatively quickly)
  2. Typically begins in lower extremities and moves proximally, BILATERAL symptoms

Possible associated features

  1. Sensory loss
  2. Severe back pain
  3. Dysautomina (ex: tachycardia, impaired BP control, loss of sweating, urinary retention)
  4. Respiratory failure
70
Q

Guillain- Barre is most commonly seen after

A

Campylobacer jejuni

71
Q

Describe the workup of Gullain Barre

A
  1. Consistent exam
  2. Lumbar puncture: increased protein without elevated WBC in CSF
    3, NCV: not necessary for diagnosis, abnormalities may not be seen for the first few weeks.
72
Q

Describe the Managment of Gullain Barre

A
  1. Need to go to hospital in case they are in the progressive phase and go into resp. failure
  2. Plasmapheresis or IVIG: speeds up recovery, does not affect eventual outcome
  3. Supportive measures (ventilation, blood pressure support, etc)
  4. Aggressive rehab
73
Q

Describe the Prognosis of Gullain Barre

A
  • 80% ambulating independently at 6 months
  • 60% recover completely in one year
  • 4-5% fatality rate
74
Q

What is an electromyelogram

A

Measurement of electric potential produced by skeletal muscle.
Almost always performed with nerve conduction study.

75
Q

spontaneous depolarization of single peripheral nerve causing synchronous contraction of all the muscle fibers in that motor unit

A

fasciuclation

76
Q

repetitive stimulation causes decreased amplitude in muscle action potential

A

Fatigability

77
Q

Describe the myopathies types

A

Myopathies: muscle fibers do not function properly

  1. Inherited
    - Examples: muscular dystrophies, mitochondrial myopathies
    - Generally progressive and not treatable
  2. Acquired
    - Often autoimmune
    - May respond to immunosuppressive therapies
78
Q

Possible presenting sx of myopathies

A
  1. Generalized weakness,
  2. twitching,
  3. fasciculation,
  4. gait abnormalities,
  5. fatigability,
  6. myalgia
  7. Often slowly progressive with non-specific presentations, may takes years to diagnose
79
Q

Describe the work up of myopathies

A
  1. Nerve-conduction studies
  2. Electromyelogram
  3. Muscle biopsy (hit or miss)
  4. MRIs if indicated to rule out other conditions
  5. Labwork looking for inflammatory markers, evidence of metabolic abnormalities
  6. Consideration of genetic testing (generally these have good specificity but poor sensitivity, only helpful if positive)
80
Q

What is M yasthenia Gravis

A

Autoimmune
Acetylcholine Receptor Antibody blocks post-synaptic acetylcholine receptor
Leads to muscle fatigability, strength improves with rest

81
Q

Subtypes of Myasthenia Gravis

A
  1. Ocular myasthenia: ptosis and impairment of EOMs only

2. Generalized myasthenia

82
Q

Sx of generalized Myasthenia

A
  1. Ocular symptoms
  2. Limb strength (weakness proximal>distal)
  3. Dysphagia
  4. Dyspnea
  • Symptoms may wax and wane in severity, remission may not last indefinitely
  • Myasthenia crisis may require hospitalization and temporary life-support.
83
Q

Describe the work up of Myasthenia Gravis

A
  1. Exam: fatigability** of skeletal muscles, ptosis, fatigability of upgaze, dyspnea
  2. EMG: decreased amplitude with repeated stimulation in affected muscles (not typically used)
  3. Labwork: ACh receptor Abs
  4. Chest Xray to evaluate for enlarged thymus gland**
  5. Tensilon test
84
Q

What is a Tensilon test

A
  1. Edrophonium: rapid acetylcholinesterase inhibitor
  2. Flood synapse with acetylcholine and should see rapid improvement in symptoms
  3. Only helpful if there is a symptom that is easy to objectively evaluate (ex: ptosis)
85
Q

Describe the Tx of Myasthenia gravis

A
  1. Pyridostigmine: increase ACh in synapse– tx sx only (GI SE)
  2. Immunosuppression (Prednisone, Imuran, Cellcept)
  3. Thymectomy if large thymus on CXR or CT- Traditionally requires sternotomy; less invasive procedures becoming more common

Adult Clinical Medicine (26 decks)

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