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Flashcards in Neuropathology 2 Deck (164)
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A: Describe [Radicular Root Pain]

B: What causes it (2)

C: What, associated with this, causes a [dull & local pain]?

A: [LSS Pain-Lightning/Stabbing/Shooting Pain] that situates itself in the dermatomal distribution of a dorsal root


1. Inflammation of [Dorsal Root]

2. Extramedullary compression of [Dorsal Root]


C: The extramedullary lesion itself


A: Clinical sensory deficits correlate to the ____[vertebrae / spinal cord] level

B: Which between the two listed above extends down longer? 

A: Clinical sensory deficits correlate to the Spinal Cord level

B: Vertebral column becomes longer than spinal cord during development


Describe the sensory signs for Spinothalamic Tract lesions (3)

  1. Contralateral deficit of pain and temp
  2. [Sacral Sparing during intramedullary lesions] (since sacral fibers are far lateral)
  3. [Deficit is up to dermatomal level in EXTRAmedullary lesions] 


A: Clinical Manifestation for [ANT Spinal Artery Occlusion] (3)

B: What types of things cause this? 


1) Sudden Hyperreflexic spastic paraparesis

2) Loss of Pain/Temp inferior to the lesion

3) Preserved [2TVP-2point/Touch/Vibration/Position]



-Atherosclerotic aortic Dz

-Aortic Surgery 


A: Describe [SuB ACute Combined Degeneration] (2)

B: What are the causes (3)

A: [Demyelinating lesions] in Posterior and Lateral Columns (usually at thoracic level) --> 

-loss of [2TVP- 2point discrimination/Touch/vibration/position] of LE

but with...

-intact Pain and Temp

B:  [SuB ACute Combined Degeneration]

1) B12 Deficiency

2) Copper Deficiency



A: Describe [ALS-Amyotrophic Lateral Sclerosis]

B: Clinical Manifestation (3)

C: Prognosis and Tx

D: Issue with diagnosing ALS

E: Breathing Evaluation (2)

A: Progressive Degeneration of [UMN Pyrimidal Betz Cells] AND [LMN ANT Horn cells AFFECTED MORE!] --> Spheroid lesions


1) Weakness affecting speech/chewing/breathing and eventually proximal limb atrophy = LMN sign

2) Fasciculations Diffusely = LMN sign

3) [Exaggerated Reflexes + Babinski] = UMN sign

C: Fatal but can give  [Riluzole (glutamate blocker)] since glutamate over exites motor neurons

D: UMN signs may be first confused with a cervical spinal cord lesion! 

E: many pts fear respiratory failure. Mitigate with: 

-Aggressive = [Tracheostomy Mechanical Ventilation]

-Supportive= [CPAP vs. BiPAP]


 Motor Neuron Disease

A:  ALS-Amyotrophic Lateral Sclerosis Pgn

B: Mode of Inheritance

A: Progressive Degeneration of [UMN Pyrimidal Betz Cells] AND [LMN ANT Horn cells Spheroid lesions & has the WORST PGN OF ALL MOTOR NEURON DISORDERS (50% Die within 3 years from respiratory failure or profound weakness)

B: [RARELY FAMILIAL (Chromo 21 Superoxide Dismutase Gene mutation) but affects more Males]



Clinical Manifestation of Tabes Dorsalis (4)

1st) Lightning pain from [initial dorsal root lesion] (from loss of DRG and dorsal root)

2nd) Loss of [2VP-2point discrimination/vibration/position] from dorsal column degeneration --> [Romberg] + [Stomping Gait] + [Charcot Joints]

3rd) Loss of ALL SENSES (from loss of DRG and dorsal root)

4th)  [Areflexia but Preserved Strength]


A: Describe the 3 main sx for [Brown Sequard Syndrome]

B: Causes (3)

1. Contralateral STT Loss of Pain/Temp

2. Ipsilateral DCP Loss of 2TVP-2point/Touch/Vibration/[Position Proprioreception]

3. Ipsilateral CST Loss --> Muscle Weakness



[(Extramedullary Tumor] vs. Trauma vs. (Herniated Disc)]


A: Pathophysiology of Myasthenia Gravis

B: When does it onset? Describe the 2 types.

C: What things are preserved in this dz? (2)

D: What is Myasthenic Fatigue

A: Autoimmune Dz that blocks and INC degradative turnover of [postsynpatic nicotinic ACh Receptors]]

B: [Generalized (more common) vs. Ocular] and occurs at ANY AGE! 

1. Generalized= P DDD WF 

[Ptosis/[Diplopia from Disconjugate gaze]/Dysarthria/Dysphagia/ [Weakness(Respiratory and limbs)/ Fatigue-especially with certain activities] ]

2. Ocular= [Ptosis/Diplopia] after 2-3 years of dx

C: Sensation and Reflexes

D: Exercise normally DEC ACh release but is compensated  by the saftey factor. 

During Myasthenia Gravis, this DEC ACh during exercise PLUS the [Loss of EPP-End Plate Potential]--> Loss of muscle depolarization --> Myasthenic Fatigue


A:  3 ways to diagnose Myasthenia Gravis

B: Which test is most specific

1. Elevated [Serum Antibody against (postsynpatic nicotinic ACh Receptors)] = MOST SPECIFIC

2.Positive [Tensilon Edrophonium] short acting AChEsterase inhibitor. If after IV injection, pt feels better = they have Myasthenia Gravis

3. EMG showing evidence of abnormal Neuromuscular junction transmission (i.e. repetitive nerve stimulation)


Myasthenia Gravis Tx (4)

  1. AntiCholinesterase drugs --> allows ACh to stick around longer
  2. Thymectomy (remove part of Thymus that contains ACh Receptor-like material)
  3. Immunosuppresants

-[Azthioprine vs. Mycophenolate Mofetil]



  4. [Plasmapheresis vs. IV Immunoglobulin]= Transient but potent fixes


A: Pathophysiology of [Lambert Eaton Myasthenic Syndrome]

B: Clinical Manifestation (3) 

C: Dx (3)

D: What CA is this syndrome associated with?

A: [Autoimmune attack against (Presynpatic Ca+ channel)--> No ACh release] 


-Fatigable weakness of Proximal limbs and trunk that mimic myopathy

-Improved briefly by exertion

-Autonomic sx (Dry mouth & Orthostasis) 


C: [Nerve Stimulation test vs. EMG vs. Ab Detection]

D: usually associated with SOLC-Small Oat cell Lung Carcinoma


[Lambert Eaton Myasthenic Syndrome] tx (3)

  1. Tx underlying CA
  2. Drugs to enhance ACh release (Guanidine vs. Diaminopyridine)
  3. Immunosuppresants


A: What is Mononeuropathy

B: Pathophysiology

C: Dx (2)

D: Examples (3)

A: Single Major "named" nerve is involved (sensory vs. motor vs. Both)

B: [Trauma or Compression] ---> focal demyelination of a nerve and possibly axonal damage if lesion is severe

C: Diagnosed with EMG and nerve testing

D: Ex: 

1. [Carpal Tunnel Median mononeuropathy] = most common! 

2. Ulnar mononeuropathy from leaning on elbow

3. Peroneal mononeropathy from [lateral knee injury]


A: [Carpal Tunnel Median mononeuropathy] pathophysiology

A2: What do severe cases of this lead to? 

B: Tx (3) 

A: is a compression mononeuropathy that occurs when [inflammed flexor tendons/fluid retention (pregnancy) / swelling] all compress the Median nerve in the carpal tunnel --> Tingling Numbness. 

A2: Severe cases = Thenar atrophy--> weakness

B: Tx


-Local Rest

-Surgery vs. Splint



What is Wallerian Degeneration? 

When the peri and epineurium are preserved after the nerve trauma the axons undergoes Wallerian Degeneration. The perserved scaffolding allows sufficient axonal sprouting and regeneration within the PNS


A: Pathophysiology of [Peripheral Polyneuropathy]

B: Clinical Manifestation of [Peripheral Polyneuropathy] (4)

A: [Disorder of multiple, major AND small n.] caused by     -axonal degeneration(will DEC EMG amplitude) and          -secondary demyelination(will DEC EMG velocity) . Both due to inadequate axoplasmic flow-->

B: 1. [early sensory loss of distal limbs (i.e. feet)]--> eventually [motor loss of distal limbs] --> atrophy--> weakness. (longest sensory cells are affected 1st)

2. [Early loss of muscle stretch reflexes]

3. Paresthesia= spontaneous tingling 

4. Dysesthesia= Unpleasant sensation from non-noxious stimulus

eventually hands are affected as well


A: Causes of [Peripheral Polyneuropathy] (4)

B: Dx (3)

  1. Hereditary
  2. Toxic (Drugs vs. Occupation)
  3. Other Multiple Mononeuropathies or autoimmune pathologies (DM vs. SLE vs. Guillain Barre)
  4. Idiopathic= MOST COMMON

B: EMG vs Blood testing vs. Nerve biopsy


Describe the EMG

Needle Electromyography. Electrical activity of muscles within 1 motor unit to be assessed for nerve damage and muscle dz


A: Describe Guillain Barre Syndrome

B: What Pt demographic is mostly affected by this

A: Acute Polyneuropathy manifesting as inflammation and demyelination of [peripheral n. and roots] --> [ascending NON-reflexic paralysis (includes respiratory paralysis)] --> [little sensory loss but some paresthesia and eventually reflex loss] 

B: Occurs at any age, but 50% of pts have [Viral URI] prior to getting Guillain Barre


Guillain Barre Syndrome

A: Dx (2)

B: Pgn

C: What tx would help accelerate recovery? 

A: Dx

1) EMG testing that reveals demyelination

2) Elevated CSF Protein and possible WBC


B: Pgn = GOOD!


C: [Plasmapheresis vs. IVIG] may shorten illness


Remember that Guillain Barre is a type of Polyneuropathy


[Chronic Acquired Polyneuropathies]

Causes (8)

[Chronic Acquired Polyneuropathies] : takes months-years to actually develop

May Destroy ​NITRIC 

  1. Metabolic/Endocrine (Uremia vs. hypOthyroid)
  2. DM
  3. Nutrition (Vitamin B Deficiency)
  4. Infection (Leprosy = MOST COMMON WORLDWIDE)
  5. Toxins (alcoholism vs. lead)
  6. Rheumatological (RA vs. Lupus)
  7. Idiopathic
  8. CA (myeloma)


Hereditary Neuropathies

A: Pathophysiology

B: When does it onset

C: Clinical Manifestation and tx

A: known or unknown metabolic vs. genetic disorders --> [Distal sensorimotor deficits with little to no paresthesia/dysesthesia] 

B: Childhood

C: Orthopedic Deformities (scoliosis/hammertoes/pes cavus): Give assistive devices, but otherwise NO TX


A: Myopathy Clinical Manifestation (3)

B: Dx (4)


1) Proximal Limb (shoulders/hips) weakness and atrophy

2) LATE loss of reflexes after muscular atrophy onsets

3) Intact sensation



-Family hx of muscualar dystrophy

-Elevated Creatinine Kinase (muscle enzyme)


-Muscle Biopsy


A: Polymyositis (Describe and List causes (4))

B: Clinical Manifestation (2)

C: Dx

D: Tx


A: A type of myopathy involving multiple muscles and caused by: 

1) Autoimmune= MOST COMMON IN USA

2) Viral 

3) Drugs

4) CA= rare


-Proximal weakness over weeks to months

-Dermatomyositis: Rash around eyes or fingers

C: *[Inflammation-mononuclear inflammatory infiltration]/necrosis on biopsy

D: Corticosteroids


 Duchenne's Muscular Dystrophy

A: pathophysiology

B: Onset

C: Clinical Manifestation (2)

A: [X-linked disorder] --> Absence of the [dystrophin muscular structural protein]--> [Cardiac / Respiratory / Proximal Limb Weakness] 

B: Boyhood


1) Calf Pseudohypertrophy (from muscle being replaced by fat & connective tissue)

2) Cardiorespiratory Death by Age 30


A: Describe Motor Neuron Disease

B: MOD for sub-type: Spinal Muscular Atrophy 

-Clinical Manifestation

-Infant type: Name and MOD

-Teen/Adult type: Pgn 

A: Degeneration of UMNLMNor both  --> varying serverity and rate of degeneration

B: [Spinal muscular atrophy] = specifically [ANT Horn Cell degeneration] from [Chromo 5 SMN1 and 2 gene mutations]--> LMN signs of FAW- Weakness/[atrophy & areflexia] /Fasciculations

*Infantile onset = (Werdnig Hoffman) --> [Auto Recessive terminal condition --> Floppy Baby from defuse [Distal muscle atrophy]

*Milder childhood/adult onset types --> [Non-fatal Chronic Disability] 


A: Clinical Manifestation of Olfactory Nerve lesion (3)

B: How are these lesions associated with Head Trauma?


1) [Sinusitis vs. URI] (most common)

2) Anosmia

3)Orbitofrontal Tumor (rare)

B: Shears nerve branches in Cribiform Plate


A: Describe the difference between Binocular Diplopia and monocular Diplopia

B: Lesion of [CN 3/4/6] produces what type of Diplopia?


Binocular= single image appears when 1 eye is covered


monocular= DOUBLE image appears when 1 eye is covered (comes from Psych dz vs. [ocular pathology i.e. dislocated lens])


B: Binocular Diplopia